Lecture 3 Flashcards

(53 cards)

1
Q

The nervous system is divided into two main branches name them and the branches under those branches

  1. What does the “separation of powers” across a membrane refer to in cell physiology?

A. Division of the nucleus and cytoplasm
B. The presence of gap junctions in the membrane
C. Unequal distribution of electrical charges across the membrane
D. The separation of organelles by membranes

  1. What creates the “potential” for the membrane to do electrical work?

A. Movement of water molecules
B. Uniform ion distribution
C. Separation of opposite charges across the plasma membrane
D. Fusion of vesicles with the membrane

  1. When does a cell have no membrane potential?

A. When there is a strong electrical gradient
B. When charges are evenly distributed on both sides
C. When Na⁺ and K⁺ are separated
D. When the membrane is impermeable

  1. Why is the membrane potential considered “potential energy”?

A. It makes the membrane more rigid
B. It can be used to drive electrical signals or transport
C. It stores energy in ATP
D. It only functions during cell division

  1. Which condition would result in the greatest membrane potential?

A. No difference in ion concentration
B. Equal permeability to all ions
C. Large difference in ion concentration and selective permeability
D. Closed ion channels

Why is the resting membrane more permeable to potassium (K⁺) than to sodium (Na⁺)?

A. Sodium ions are smaller and move faster
B. There are more open potassium channels than sodium channels
C. Potassium ions are actively pumped out of the cell
D. Sodium channels are always open at rest

A

The CNS and PNS

CNS is divided into brain and spinal cord
PNS is divided into somatic and autonomic.
Somatic is divided into sensory and motor
Autonomic is divided into sympathetic and parasympathetic and enteric

Enteric Nervous System:

•	A distinct branch of the autonomic nervous system that operates mostly independently, sometimes called the “second brain” or “gut brain.”

The parasympathetic system is under direct control of the brain and spinal cord, whereas the enteric system can operate independently of the brain but can be influenced by sympathetic and parasympathetic signals
• Functions: The parasympathetic system broadly regulates the body’s energy conservation and homeostasis, while the enteric system specifically manages digestive functions.
• Areas of influence: Parasympathetic activity affects many organs throughout the body, while the enteric system is localized to the gastrointestinal tract.

Here are the correct answers and explanations for each MCQ:

  1. What does the “separation of powers” across a membrane refer to in cell physiology?

Correct answer: C. Unequal distribution of electrical charges across the membrane
Explanation:
This “separation of powers” is not political but physiological—it refers to separating positive and negative charges across the plasma membrane, creating an electrical gradient (membrane potential).

  1. What creates the “potential” for the membrane to do electrical work?

Correct answer: C. Separation of opposite charges across the plasma membrane
Explanation:
When charges are separated, they can be allowed to move (like opening a channel), releasing energy that can be used for work like nerve impulse transmission or muscle contraction.

  1. When does a cell have no membrane potential?

Correct answer: B. When charges are evenly distributed on both sides
Explanation:
If the charge on the inside and outside of the cell is the same, there is no electrical gradient—no stored energy to drive movement, so the membrane potential is zero.

  1. Why is the membrane potential considered “potential energy”?

Correct answer: B. It can be used to drive electrical signals or transport
Explanation:
It’s called “potential” because it’s stored energy that can be used for action potentials, secondary active transport, etc., once channels open and ions flow down their gradient.

  1. Which condition would result in the greatest membrane potential?

Correct answer: C. Large difference in ion concentration and selective permeability
Explanation:
A steep concentration gradient plus selective permeability (e.g., K⁺ leaks out but negative proteins stay in) creates a strong charge difference = strong membrane potential.

Why is the resting membrane more permeable to potassium (K⁺) than to sodium (Na⁺)?

A. Sodium ions are smaller and move faster
B. There are more open potassium channels than sodium channels
C. Potassium ions are actively pumped out of the cell
D. Sodium channels are always open at rest

Correct answer: B. There are more open potassium channels than sodium channels

Explanation:
At rest, more K⁺ leak channels are open compared to Na⁺ channels, so K⁺ diffuses out more easily, making the membrane more permeable to K⁺. This contributes to the negative resting membrane potential.

Distribution of lons Across the Plasma Membrane due to lon channels
• Nat and K+ can passively diffuse across the membrane through specific protein channels
At resting membrane potential, the membrane is much more permeable to K+ than to Nat because the cell has many more channels open for passive K+ traffic than for passive Na+ traffic

Sodium (Na⁺) and potassium (K⁺) passively diffuse across the membrane through leak channels:

Specific channels:
1. Potassium leak channels (K⁺ leak channels)
• Always open
• Allow K⁺ to leak out of the cell
• Responsible for the high K⁺ permeability at rest
2. Sodium leak channels (Na⁺ leak channels)
• Fewer in number
• Allow limited Na⁺ to leak in
• Contribute slightly to the resting membrane potential

These are non-gated (always open) channels that allow passive diffusion based on the electrochemical gradient.

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2
Q

How many neurons are in the brain

Explain separation of powers and how it affects membrane potential ( when will we say there is a potential?)

A

100 billion neurons
~ 104 synapses/ neuron
~ Trillions of synapses

All living cells have a plasma membrane potential (electrical polarization), which is measured in millivolts (mV).
Separation of opposite charges across plasma membrane allows a “potential” to do work.
When oppositely changed particles have been separated, the electrical force of attraction between them can be harvested to perform work once they are permitted to come together again (“potential” to do work).
The membrane potential is due to differences in concentration and permeability of key ions.
Inside cell: negative; Outside cell: positive

Membrane Potential = Electrical Potential Energy
• It exists when there is a separation of opposite charges across the plasma membrane.
• Ions like Na⁺, K⁺, and Cl⁻ are unequally distributed inside and outside the cell.
• This unequal distribution + selective membrane permeability (via ion channels/pumps) creates a voltage (potential) across the membrane.

When the Cell Has Membrane Potential:
• There is a separation of charge across the membrane:
• More positive charges outside, more negative charges inside.
• This creates an electrical gradient, usually around –70 mV in neurons (resting membrane potential).
• The cell is said to have “potential” energy, which can be used for nerve signals, muscle contraction, etc.

When the Cell Has No Membrane Potential:
• There is no charge difference across the membrane:
• Ions are evenly distributed on both sides.
• No electrical force exists to drive ion movement.
• This is called depolarization to zero or electrical neutrality.
• In this state, the cell has no potential to do electrical work.

So for a membrane to have potential, for the outside, it’s supposed to be more positive than the inside and for the inside, it’s supposed to be more negative than the outside. Example is outside (15+,10-) and inside being (15-,10+)

Your example works:
• Outside: 15 positive, 10 negative → Net: +5
• Inside: 15 negative, 10 positive → Net: –5

This separation of charges creates a voltage difference (membrane potential). The cell now has potential to do electrical work, like sending nerve impulses.

If both sides had equal net charges (e.g., +5 inside and +5 outside), then no membrane potential would exist

Exactly — that’s a perfect example.

In this case:
• Outside: 10 positive, 10 negative → Net charge = 0
• Inside: 10 positive, 10 negative → Net charge = 0

There is no difference in charge across the membrane, so the membrane potential = 0 mV.
This means no electrical gradient, and the cell has no stored electrical energy for work.

That’s what we mean when we say the cell has no membrane potential.

Would you like a quick table summarizing different scenarios for clarity?

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3
Q

Apart from neurons, the brain is made up of glial cells.
State the 4 types of glial cells and their functions
Which of these types is the most abundant glial cells
What is the blood brain barrier

A
  1. Astrocytes: most abundant glial cells and make contact with all surfaces
    • Functions: Provide structural support, responsible for metabolic activities in the brain such as glucose metabolism, maintain the blood-brain barrier(managing the kind of things that enter the blood brain barrier and what goes out) , regulate blood flow, influence synaptic activity, and manage ion balance and neurotransmitter recycling.
    • Location: Found throughout the brain and spinal cord.
    1. Oligodendrocytes:
      • Functions: Produce myelin in the central nervous system, which insulates axons or neurons and enhances the speed of electrical signal transmission.
      • Location: Predominantly in the white matter of the brain and spinal cord.
    2. Microglia: they police the brain
      • Functions: Act as the primary immune cells of the central nervous system, engaging in phagocytosis to remove debris, damaged neurons, and pathogens. They also play a role in inflammation and repair processes.
      • Location: Scattered throughout the brain and spinal cord.
    3. Ependymal Cells:
      • Functions: Line the ventricles of the brain and the central canal of the spinal cord. They produce and circulate cerebrospinal fluid (CSF) through their cilia.ependymal cells form a blood CSF barrier
      • Location: Within the ventricles of the brain and the central canal of the spinal cord.

Neurones need metabolic support

Blood vessels lined with endothelial cells with tight junctions ensure an adequate energy supply to the brain as well as a protective barrier (blood-brain barrier)

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4
Q

State six functions of the brain

A

Cognition: learning, memory, decision-making etc
Movement, posture and balance
Regulation of heart rate, blood pressure etc
Hunger and satisfaction
Hormonal regulation
Sleep and circadian rhythms
Reproduction (sex etc.)
Sensations like pain, touch etc
Vision, hearing, olfaction, taste
Emotions: happiness, reward and punishment

The brain is, perhaps,… MTN

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5
Q

State three basic functions of the nervous system(not just the brain)

Which of the following best describes the electrochemical gradient that drives ion diffusion through open channels?

A. It is created only by the electrical charge difference across the membrane
B. It is the combination of concentration and electrical gradients across the membrane
C. It requires ATP to move ions through the channel
D. It only applies to neutral molecules, not ions

What is the role of the electrical driving force in ion movement through an open channel?

A. It pumps ions against their concentration gradient
B. It only affects uncharged molecules
C. It causes opposite charges to repel each other
D. It attracts opposite charges and repels like charges

When do the chemical and electrical driving forces act in the same direction?

A. When the ion is neutral
B. When the ion is pumped using energy
C. When both the concentration gradient and electrical gradient favor the same direction of movement
D. When the membrane potential is zero

The potential difference generated across a membrane results from what?
State the two criteria needed to achieve diffusion potential

State the four main types of diffusion potential (the explanations are at the end)

A

.Sensory Function
- Detection of both internal and external stimuli

• Interpretive Function
- Analyzes, stores, and makes decisions based on sensory information

• Motor Function (Response)
— Response to interpretive data

Diffusion Potential of Electrolytes
• Potential difference generated across a membrane resulting from:
• Unequal diffusion of positive and negative ions
• Two criteria to achieve diffusion potential:
• Concentration gradient across the membrane
• Selective permeability of membrane
• Diffusion potential is created by movement of few ions which end up creating large changes in membrane potential.

Which of the following best describes the electrochemical gradient that drives ion diffusion through open channels?

A. It is created only by the electrical charge difference across the membrane
B. It is the combination of concentration and electrical gradients across the membrane
C. It requires ATP to move ions through the channel
D. It only applies to neutral molecules, not ions

Correct answer: B. It is the combination of concentration and electrical gradients across the membrane

Explanation:
• The electrochemical gradient combines:
• Chemical gradient (difference in ion concentration)
• Electrical gradient (difference in charge)
• Ions move passively through open channels according to this combined force.

What is the role of the electrical driving force in ion movement through an open channel?

A. It pumps ions against their concentration gradient
B. It only affects uncharged molecules
C. It causes opposite charges to repel each other
D. It attracts opposite charges and repels like charges

Correct answer: D. It attracts opposite charges and repels like charges

Explanation:
Negative areas attract positive ions and repel negative ions, and vice versa. This electrical force influences how ions move across the membrane.

  1. When do the chemical and electrical driving forces act in the same direction?

A. When the ion is neutral
B. When the ion is pumped using energy
C. When both the concentration gradient and electrical gradient favor the same direction of movement
D. When the membrane potential is zero

Correct answer: C. When both the concentration gradient and electrical gradient favor the same direction of movement

Explanation:
The chemical and electrical forces can work together (same direction) or oppose each other. When they work together, ion movement is faster and easier.

Note: Driving forces for Diffusion of lons through an Open Channel
Chemical driving force = the concentration gradient across the membrane
Electrical driving force = separation of charges causes an electrical gradient across the membrane
negative areas tend to attract positive ions and repel negative ions, and vice versa
Combined these forces lead to an electrochemical gradient.
Note that chemical and electrical forces can act in the same or opposite directions.
Diffusion of an ion through an open shannel is passive and requires no energy expenditure.

Types of Diffusion Potential
• Equilibrium Potential
• Resting membrane potential
• Graded Potential
• Action Potential

Of course! Here’s a much simpler version:

  1. Equilibrium Potential

The point where an ion stops moving in or out. Balance between charge and concentration.

  1. Resting Membrane Potential

The normal state of the cell when it’s not active. Inside is more negative than outside.

  1. Graded Potential

A small change in charge that happens near where a signal starts. It can grow or fade.

  1. Action Potential

A big, fast change in charge that travels down the cell. It happens when the signal is strong enough.

Let me know if you’d like even shorter one-line versions!

Or:

Sure! Here are two short sentences for each type of diffusion potential:

  1. Equilibrium Potential

It is the membrane potential at which there is no net movement of a specific ion. It reflects the balance between that ion’s concentration gradient and electrical gradient.

  1. Resting Membrane Potential

This is the steady voltage difference across the membrane of a resting (non-excited) cell, typically around -70 mV. It is mainly due to K⁺ leak channels and Na⁺/K⁺ pump activity.

  1. Graded Potential

These are small, localized changes in membrane potential that vary with stimulus strength. They can either depolarize or hyperpolarize the membrane and fade with distance.

  1. Action Potential

A rapid, large, and brief change in membrane potential that travels along excitable cells like neurons. It occurs when a threshold is reached, causing voltage-gated Na⁺ and K⁺ channels to open in sequence.

Would you like these summarized further into flashcard form?

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6
Q

What is the morphology of a nerve cell or state the six main parts of the nerve cell
Which part of the nerve cell doesn’t have nissl granules. Which part has a lot of it?
What are nissl granules?
Look at picture of the nerve cell in the slide after trying to answer
What is a synapse? A synapse contains what three things?
Where are action potentials generated from at the start?
What is the function of the axon terminal or terminal bouton

A

Generally the nerve cell is divided into the soma part and the axonal part.

-Axon hillock: The axon hillock is a specialized region of the neuron where the cell body transitions into the axon. Action potentials is propagated from or initiated at. - It is located at the junction between the cell body (soma) and the axon.
- The axon hillock is characterized by a lack of Nissl bodies, making it appear clear when stained and viewed under a microscope.
-Nucleus
-Nissi granules in the cytoplasm : Nissl Granules
Nissl granules, also known as Nissl bodies, are structures found within the cell body (soma) and dendrites of neurons.
- Nissl granules are composed of rough endoplasmic reticulum (RER) and ribosomes. The abundance of Nissl granules reflects the high metabolic activity of neurons

-. Cell Body (Soma):
- Contains the nucleus and organelles (such as the endoplasmic reticulum, Golgi apparatus, and mitochondria).
- Responsible for maintaining the cell’s health and metabolic activities.
- Acts as the main site for protein synthesis and other cellular processes.

-Dendrites**:
- Branched, tree-like extensions from the cell body. It connects to other nerve cells
- Receive incoming signals from other neurons and transmit them toward the cell body.
- Contain receptors for neurotransmitters released by other neurons( so they can receive the information from the neurotransmitters or signals from the neurotransmitters released by other neurons)

-Axon**:
- A long, thin projection that transmits signals away from the cell body to other neurons, muscles, or glands.
- Can vary in length from less than a millimeter to over a meter in some cases (e.g., the sciatic nerve).
- The axon hillock is the area where the axon joins the cell body and is typically the site where action potentials are initiated.

  1. Myelin Sheath:
    • A fatty layer that insulates the axon and speeds up the transmission of electrical signals.
    • Formed by glial cells: oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system.
    • The myelin sheath is segmented, with gaps called nodes of Ranvier.
  2. Nodes of Ranvier:
    • Gaps in the myelin sheath where the axon membrane is exposed.
    • Allow for saltatory conduction, where the action potential jumps from node to node, greatly increasing the speed of signal transmission.
  3. Axon Terminals (Synaptic Boutons):
    • The ends of the axon that make synaptic contacts with other neurons or effector cells.
    • Contain synaptic vesicles filled with neurotransmitters, which are released into the synaptic cleft to transmit signals to the next cell. Yes, axon terminals and terminal boutons refer to the same structure in a neuron.
  • Axon Terminals: These are the distal endings of an axon, where the neuron makes synaptic connections with other neurons, muscle cells, or glands.
  • Terminal Boutons: This term specifically describes the small, bulb-like structures at the very end of the axon terminals. These boutons contain neurotransmitters that are released into the synaptic cleft to communicate with the next cell.

In essence, “terminal boutons” is a more detailed term referring to the small structures found at the axon terminals.

  1. Synapse:
    • synapse is a specialized junction where a neuron communicates with another cell, which can be another neuron, a muscle cell, or a gland cell
    • Includes the presynaptic membrane, synaptic cleft, and postsynaptic membrane.
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7
Q

What are the two main types of synapses
Which is more common and why
Which is faster

Why does the action potential only travel in one direction along a neuron?
• a) Because sodium channels behind the action potential are inactivated
• b) Because potassium channels are only present at the axon terminal
• c) Because neurotransmitters prevent backward movement
• d) Because the myelin sheath blocks backward conduction

Which factor does not significantly contribute to the resting membrane potential?
• a) Sodium-potassium pump
• b) Leak channels
• c) Intracellular anions
• d) Voltage-gated calcium channels

Which of the following conditions will lead to hyperpolarization of a neuron?
• a) Increased extracellular sodium concentration
• b) Increased permeability to chloride ions
• c) Increased intracellular potassium concentration
• d) Increased permeability to sodium ions

Why does the action potential have an all-or-none characteristic?
• a) Because it depends on the strength of the stimulus
• b) Because it only occurs if the membrane potential reaches the threshold
• c) Because it varies with the duration of the stimulus
• d) Because it can be partially activated

How does the sodium-potassium pump contribute to the maintenance of the resting membrane potential?
• a) By passively allowing ions to move according to their gradients
• b) By actively transporting sodium out of the cell and potassium into the cell
• c) By blocking all ion movement across the membrane
• d) By generating action potentials

Which protein complex is directly involved in the fusion of synaptic vesicles with the presynaptic membrane?
• a) SNARE complex
• b) GABA receptor
• c) Na+/K+ ATPase
• d) Voltage-gated sodium channel

Which of the following processes is directly involved in the recycling of synaptic vesicles?
• a) Exocytosis
• b) Endocytosis
• c) Transcytosis
• d) Phagocytosis

What is the primary function of synaptotagmin in synaptic vesicle fusion?
• a) Sensing calcium levels
• b) Binding to neurotransmitters
• c) Transporting sodium ions
• d) Forming the vesicle membrane

During synaptic transmission, which process follows the fusion of synaptic vesicles with the presynaptic membrane?
• a) Binding of neurotransmitters to postsynaptic receptors
• b) Depolarization of the presynaptic terminal
• c) Influx of potassium ions into the presynaptic terminal
• d) Breakdown of the synaptic vesicle membrane

36.	What would happen to the resting membrane potential if the cell membrane became equally permeable to sodium and potassium ions?
•	a) It would become more negative
•	b) It would become more positive
•	c) It would remain unchanged
•	d) It would oscillate
A

There are two main types of synapses: chemical synapses and electrical synapses. Here, we’ll focus on the more common chemical synapses:
Electrical synapses are faster. This is because electrical synapses involve direct current flow between cells through gap junctions, allowing for almost instantaneous transmission of signals.

Direct Current Flow: Electrical synapses transmit signals via gap junctions that allow ions to pass directly between adjacent cells. This means the signal is passed with minimal delay and without the need for neurotransmitters. However, this also means there is less opportunity for modulation

But chemical synapses are more common because they allow more complex signaling . Neurotransmitters can activate different different types of receptors on the postsynaptic cell leading to different responses. They also allow for modulation of the signaling. The amount of neurotransmitters being released can be controlled while in electrical synapses, it’s less easy to control the signaling.
Structure of a Chemical Synapse

1.	Presynaptic Neuron:
•	Axon Terminal: The end of the axon of the presynaptic neuron.
•	Synaptic Vesicles: Membrane-bound sacs in the axon terminal that contain neurotransmitters.
•	Presynaptic Membrane: The membrane of the axon terminal that faces the synaptic cleft.
2.	Synaptic Cleft:
•	A small gap (about 20-40 nanometers wide) between the presynaptic and postsynaptic membranes.
•	Neurotransmitters are released into this space.
3.	Postsynaptic Cell:
•	Postsynaptic Membrane: The membrane of the postsynaptic cell (which can be a neuron, muscle cell, or gland cell).
•	Receptors: Proteins on the postsynaptic membrane that bind neurotransmitters.

Function of a Chemical Synapse

1.	Neurotransmitter Release:
•	When an action potential reaches the axon terminal of the presynaptic neuron, it triggers the opening of voltage-gated calcium channels.
•	Calcium ions enter the axon terminal, prompting synaptic vesicles to fuse with the presynaptic membrane and release their neurotransmitter content into the synaptic cleft through exocytosis.
2.	Neurotransmitter Binding:
•	Neurotransmitters diffuse across the synaptic cleft and bind to specific receptors on the postsynaptic membrane.
•	This binding causes ion channels to open or close, leading to changes in the postsynaptic cell’s membrane potential.
3.	Signal Transmission:
•	Depending on the type of neurotransmitter and receptor, the postsynaptic cell may become depolarized (excited) or hyperpolarized (inhibited).
•	If the postsynaptic cell is a neuron and the signal is strong enough, it can generate an action potential that propagates along its axon.
4.	Neurotransmitter Clearance:
•	To terminate the signal, neurotransmitters are removed from the synaptic cleft through reuptake into the presynaptic neuron, enzymatic degradation, or diffusion away from the synapse.

Types of Synapses

1.	Chemical Synapses:
•	Most common type.
•	Utilize neurotransmitters to relay signals across the synaptic cleft.
2.	Electrical Synapses:
•	Less common.
•	Use gap junctions to allow direct electrical communication between neurons.
•	Allow ions and small molecules to pass directly from one cell to another, enabling rapid and synchronous transmission of signals.

Why does the action potential only travel in one direction along a neuron?
• a) Because sodium channels behind the action potential are inactivated
• b) Because potassium channels are only present at the axon terminal
• c) Because neurotransmitters prevent backward movement
• d) Because the myelin sheath blocks backward conduction
Answer: a) Because sodium channels behind the action potential are inactivated

Which factor does not significantly contribute to the resting membrane potential?
• a) Sodium-potassium pump
• b) Leak channels
• c) Intracellular anions
• d) Voltage-gated calcium channels
Answer: d) Voltage-gated calcium channels

Leak channels are a type of ion channel found in cell membranes that allow ions to pass through continuously, without the need for external signals like voltage changes or ligand binding. These channels are always open, permitting ions to “leak” across the membrane down their electrochemical gradient, which contributes to the maintenance of the resting membrane potential in cells.

Which of the following conditions will lead to hyperpolarization of a neuron?
• a) Increased extracellular sodium concentration
• b) Increased permeability to chloride ions
• c) Increased intracellular potassium concentration
• d) Increased permeability to sodium ions
Answer: b) Increased permeability to chloride ions

In this case, the correct answer is (b) Increased permeability to chloride ions because chloride ions (Cl⁻) are negatively charged. When a neuron becomes more permeable to chloride ions, more Cl⁻ will enter the neuron, making the inside more negative and leading to hyperpolarization (moving the membrane potential further away from zero, typically below the resting potential of around -70 mV).

While potassium ions (K⁺) also contribute to hyperpolarization, this is only true when potassium exits the cell. However, the option given is increased intracellular potassium concentration (which implies K⁺ staying inside or even entering the cell), which would make the inside of the cell less negative, not more negative.

For hyperpolarization to occur via potassium, it would have to involve increased permeability to potassium, allowing K⁺ to flow out of the cell, further driving the cell’s interior to a more negative state.

Thus, chloride influx is the best explanation in this context, as increased Cl⁻ permeability directly leads to hyperpolarization by increasing the negative charge inside the neuron.

Why does the action potential have an all-or-none characteristic?
• a) Because it depends on the strength of the stimulus
• b) Because it only occurs if the membrane potential reaches the threshold
• c) Because it varies with the duration of the stimulus
• d) Because it can be partially activated
Answer: b) Because it only occurs if the membrane potential reaches the threshold

How does the sodium-potassium pump contribute to the maintenance of the resting membrane potential?
• a) By passively allowing ions to move according to their gradients
• b) By actively transporting sodium out of the cell and potassium into the cell
• c) By blocking all ion movement across the membrane
• d) By generating action potentials
Answer: b) By actively transporting sodium out of the cell and potassium into the cell
36. What would happen to the resting membrane potential if the cell membrane became equally permeable to sodium and potassium ions?
• a) It would become more negative
• b) It would become more positive
• c) It would remain unchanged
• d) It would oscillate
Answer: b) It would become more positive

The correct answer is (b) It would become more positive because if the cell membrane became equally permeable to sodium (Na⁺) and potassium (K⁺) ions, the resting membrane potential would shift toward a more positive value.

  • Resting Membrane Potential is typically around -70 mV in neurons, largely due to the high permeability of the membrane to potassium ions (K⁺) compared to sodium ions (Na⁺). This is because K⁺ leak channels allow more K⁺ to exit the cell, keeping the inside of the cell more negative.
  • Sodium ions (Na⁺), however, have a much more positive equilibrium potential (about +60 mV), meaning if the membrane became highly permeable to Na⁺, sodium would rush into the cell, making the inside more positive.
  • In a typical resting neuron, K⁺ permeability is much higher than Na⁺, so the resting membrane potential is close to the equilibrium potential of K⁺ (around -90 mV). However, if the membrane became equally permeable to Na⁺ and K⁺, the membrane potential would be influenced by both ions equally.

Since the equilibrium potential of Na⁺ is much more positive than K⁺, the membrane potential would shift closer to 0 mV or even become slightly positive. This shift would be toward the positive side because sodium influx (positive charge) would dominate over potassium efflux (removal of positive charge).

The resting membrane potential would become more positive because Na⁺, which has a higher positive equilibrium potential, would significantly contribute to the membrane potential if its permeability increased to be equal to that of K⁺.

Which of the following processes is directly involved in the recycling of synaptic vesicles?
• a) Exocytosis
• b) Endocytosis
• c) Transcytosis
• d) Phagocytosis
Answer: b) Endocytosis

What is the primary function of synaptotagmin in synaptic vesicle fusion?
• a) Sensing calcium levels
• b) Binding to neurotransmitters
• c) Transporting sodium ions
• d) Forming the vesicle membrane
Answer: a) Sensing calcium levels

During synaptic transmission, which process follows the fusion of synaptic vesicles with the presynaptic membrane?
• a) Binding of neurotransmitters to postsynaptic receptors
• b) Depolarization of the presynaptic terminal
• c) Influx of potassium ions into the presynaptic terminal
• d) Breakdown of the synaptic vesicle membrane
Answer: a) Binding of neurotransmitters to postsynaptic receptors

Which protein complex is directly involved in the fusion of synaptic vesicles with the presynaptic membrane?
• a) SNARE complex
• b) GABA receptor
• c) Na+/K+ ATPase
• d) Voltage-gated sodium channel
Answer: a) SNARE complex

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8
Q

What is an action potential
Explain the process of action potential in a muscle cell or a nerve cell
What is the normal resting membrane potential?
What causes depolarization of the cel?
What causes repolarization of the cell
What is the falling phase of an action potential?

A

The sudden fast change in electrical potential or charge that is associated or that occurs with the passage of an impulse along the membrane of a muscle cell or nerve cell.
- It is a sudden, fast, transitory(temporary or short lived), and propagating(moves through the entire cell) change of the resting membrane potential. After the change, the cell returns to it regular resting state.
Depolarisation and opening of Na channels
Membrane potential is driven towards ENa
Na channels are gradually inactivated, while more K channels open
The membrane is now repolarized.
At the end of the AP, there is a period of hyperpolarisation

Action Potential Phases

1.	Resting Membrane Potential:
•	The resting membrane potential is the voltage difference across the cell membrane when the cell is not transmitting an impulse. It is typically around -70 mV in neurons. Associate the number 70 with the idea of resting or calm:

•	Think of the retirement age being around 70, a time of rest.
•	Or imagine a person calmly resting at 70 years old, reinforcing the idea that the cell’s resting state is at -70 mV. Also because more potassium which is -ve is in the cell( on a regular). The voltage difference across the cell membrane, also known as the membrane potential, refers to the difference in electrical charge between the inside and the outside of a cell. In neurons, this voltage difference is typically around -70 millivolts (mV), meaning the inside of the cell is 70 mV more negative than the outside when the cell is at rest (not transmitting an impulse).

Explanation:

1.	Separation of Charges:
•	The cell membrane separates ions (charged particles) inside and outside the cell. This separation of charges creates an electrical gradient.
•	The inside of the cell contains more negatively charged ions, mainly due to large proteins and the higher concentration of potassium ions (K⁺) compared to the outside. Leak channels, especially potassium leak channels, allow K⁺ ions to diffuse out of the cell more freely than Na⁺ can diffuse in, further contributing to the negative charge inside.
3.	Electrochemical Gradient:
•	This voltage difference represents the balance between the concentration gradients (the difference in ion concentrations inside vs. outside the cell) and the electrical gradients (the tendency of opposite charges to attract and like charges to repel).
•	At rest, the neuron maintains a relatively stable voltage difference, with more negative charge inside compared to the outside.

How dispersed the ions are in and outside of the cell. Net charge between extra cellular fluid and intracellular fluid. A change in the resting memerbane potential is what will cause an action potential to be propagated along the membrane of the nerve cell.
• This potential is maintained by the sodium-potassium pump (Na+/K+ ATPase), which pumps three sodium ions out of the cell and two potassium ions into the cell, and by the relative permeability of the membrane to potassium ions.
2. Depolarization:
• When a stimulus reaches a threshold level, voltage-gated sodium (Na+) channels open rapidly.
• Sodium ions rush into the cell due to the electrochemical gradient, causing the membrane potential to become more positive (toward the equilibrium potential of sodium, , which is around +60 mV).
• This rapid influx of sodium ions depolarizes the membrane, leading to the rising phase of the action potential.
3. Peak of Action Potential:
• The membrane potential approaches but does not reach because the Na+ channels begin to inactivate shortly after opening.
• At this peak, the inside of the cell is positively charged relative to the outside.
4. Repolarization:
• As the Na+ channels inactivate, voltage-gated potassium (K+) channels open.
• Potassium ions flow out of the cell, driven by their electrochemical gradient, causing the membrane potential to become more negative and return toward the resting potential. Ion Distribution and Permeability:
• Inside the cell, there is a high concentration of potassium ions (K+) and negatively charged proteins and other anions.
• Outside the cell, there is a high concentration of sodium ions (Na+) and chloride ions (Cl-). As potassium ions move out of the cell down their concentration gradient, they leave behind negatively charged proteins and other anions that cannot cross the membrane.
• This movement of positive K+ ions out of the cell makes the inside of the cell more negative relative to the outside.
• This phase is the falling phase of the action potential.
5. Hyperpolarization (Afterhyperpolarization):
• The K+ channels remain open longer than necessary, causing an overshoot and making the membrane potential more negative than the resting potential.
• This period is known as hyperpolarization or the afterhyperpolarization phase.
• Eventually, the K+ channels close, and the membrane potential returns to the resting level, reestablishing the resting membrane potential.

Yes, the action potential in neurons and muscle cells is primarily based on the movement of sodium (Na⁺) and potassium (K⁺) ions across the cell membrane. Here’s a step-by-step overview of how an action potential occurs:

  • The neuron is at its resting membrane potential, typically around -70 mV.
  • The inside of the cell is negatively charged relative to the outside.
  • Sodium and potassium channels are closed.
  • The Na⁺/K⁺ pump helps maintain this resting potential by pumping 3 Na⁺ out of the cell and 2 K⁺ into the cell.
  • A stimulus causes the membrane potential to become less negative (depolarizes) and reaches a threshold, typically around -55 mV.
  • Voltage-gated sodium channels open rapidly.
  • Na⁺ rushes into the cell due to its electrochemical gradient.
  • The influx of Na⁺ causes the membrane potential to become positive, peaking around +30 to +40 mV.
  • At the peak of the action potential, voltage-gated sodium channels inactivate.
  • Voltage-gated potassium channels open.
  • K⁺ rushes out of the cell, driven by its electrochemical gradient.
  • The efflux of K⁺ causes the membrane potential to become negative again.
  • The membrane potential temporarily becomes more negative than the resting potential due to the continued efflux of K⁺ (hyperpolarization).
  • This is because K⁺ channels are slow to close.
  • Voltage-gated potassium channels close.
  • The Na⁺/K⁺ pump and other ion channels restore the resting membrane potential.
  • The neuron is now ready for another action potential.
  • Depolarization is caused by the influx of Na⁺.
  • Repolarization is caused by the efflux of K⁺.
  • The action potential is a rapid, temporary change in the membrane potential that propagates along the axon, allowing neurons to transmit electrical signals over long distances.
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9
Q

What is a refractory period?
What are the types of refractory periods in action potentials

A

The refractory period is a crucial aspect of action potentials in neurons and muscle cells. It refers to the period of time following an action potential during which a neuron or muscle cell is less excitable and less likely to generate another action potential. There are two types of refractory periods: the absolute refractory period and the relative refractory period.

  • Definition: During the absolute refractory period, it is impossible for another action potential to be initiated, regardless of the strength of the incoming stimulus.
  • Cause: This occurs because the voltage-gated sodium (Na+) channels, which opened to initiate the action potential, become inactivated. They cannot reopen until the membrane potential returns to near the resting state and the Na+ channels have reset.
  • Duration: The absolute refractory period typically lasts about 1-2 milliseconds following the initiation of the action potential.
  • Importance: This period ensures that each action potential is a discrete, all-or-nothing event and helps to enforce the unidirectional one way propagation of the action potential along an axon.

So in absolute, it occurs right at the peak of the action potential where sodium channels are inactivated and ends in the early stages of repolarization. This period end when a significant number of sodium channels have recovered from the inactivation and have closed completely.
### 2. Relative Refractory Period
- Definition: During the relative refractory period, another action potential can be initiated, but it requires a stronger-than-normal stimulus to do so.
- Cause: This period corresponds to the time when voltage-gated potassium (K+) channels are still open, and the membrane is hyperpolarized (more negative than the resting potential). Additionally, some Na+ channels may still be in the process of resetting.
- Duration: The relative refractory period follows the absolute refractory period and lasts for several milliseconds.
- Importance: This period allows the neuron to limit the frequency of action potentials and contributes to the precise timing of signal transmission.

Relative Refractory period starts in the latter stages of the repolarization after the absolute own. It needs a stronger than normal stimulus to occur cuz the membrane potential is far away from threshold potential.

Slow Closing of Potassium Channels:
• The slow closing of K⁺ channels means that they remain open for a longer period than Na⁺ channels. As a result, K⁺ continues to exit the cell even after the membrane potential begins to drop.this leads to hyperpolarization

  • Absolute Refractory Period: No new action potential can be initiated, regardless of stimulus strength. Ensures unidirectional propagation of the action potential and maintains the integrity of the signal.
  • Relative Refractory Period: A stronger-than-normal stimulus is required to initiate a new action potential. Helps control the frequency of action potentials and fine-tunes signal timing.

These refractory periods are essential for the proper functioning of neurons and muscle cells, allowing them to reset and prepare for subsequent action potentials while maintaining the fidelity and directionality of signal transmission. Refractory Period: Ensures unidirectional propagation of the action potential and prevents immediate reactivation of the Na⁺ channels.

Return to Resting Potential

•	Na⁺/K⁺ Pump: Restores and maintains the resting membrane potential by pumping Na⁺ out and K⁺ in.
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10
Q

Explain what happens at the synapse at the nerve terminal

A

At the nerve terminal, there is supposed to be exchange of Sodium potassium and other things as well as stimulus but it doesn’t have a membrane that continues to the other nerve membrane or the other cell. The stimulus could be excitatory (it will propagate action potential to the next cell) or inhibitory (it wouldn’t propagate action potential to the next nerve cell)

Certainly! Here’s a more detailed explanation incorporating the excitatory and inhibitory aspects at the synapse:

  1. Neurotransmitter Release: When an action potential reaches the presynaptic terminal, it triggers the release of neurotransmitter molecules from synaptic vesicles into the synaptic cleft.
  2. Neurotransmitter Binding: Neurotransmitters diffuse across the synaptic cleft and bind to specific receptor molecules on the postsynaptic membrane.
  3. Postsynaptic Response:
    • Excitatory Synapses: Neurotransmitters like glutamate bind to excitatory receptors (e.g., AMPA receptors) on the postsynaptic membrane, causing depolarization (reduction in the membrane potential towards zero). This depolarization increases the likelihood that the postsynaptic neuron will fire an action potential.
    • Inhibitory Synapses: Neurotransmitters such as GABA (gamma-aminobutyric acid) or glycine bind to inhibitory receptors (e.g., GABA receptors) on the postsynaptic membrane, causing hyperpolarization (increase in the membrane potential away from zero). This hyperpolarization decreases the likelihood that the postsynaptic neuron will fire an action potential.
  4. Termination of Neurotransmission: To ensure precise signaling, neurotransmission is terminated through mechanisms such as reuptake into the presynaptic terminal, enzymatic degradation in the synaptic cleft, or diffusion away from the synapse.
  5. Integration of Signals: The postsynaptic neuron integrates excitatory and inhibitory signals from multiple synapses. The balance between excitatory and inhibitory inputs determines whether the neuron will reach its threshold for firing an action potential.

These processes are crucial for neural communication, allowing for the transmission of information across synapses in the nervous system while maintaining the delicate balance between excitation and inhibition necessary for proper brain function.

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11
Q

What is the role of calcium and sodium in Neuro transmission

A

At the synapse, the exchange of ions like sodium (Na+) and calcium (Ca2+) plays a crucial role in neurotransmission. Here’s how these ions are involved:

  1. Sodium (Na+):
    • Action Potential Propagation: When an action potential reaches the presynaptic terminal, voltage-gated calcium channels open, allowing calcium ions to enter the terminal.
    • Neurotransmitter Release: The influx of calcium ions triggers the fusion of synaptic vesicles containing neurotransmitters with the presynaptic membrane, leading to neurotransmitter release into the synaptic cleft.
    • Postsynaptic Response: After neurotransmitter release, sodium channels on the postsynaptic membrane may open in response to neurotransmitter binding, allowing sodium ions to enter the postsynaptic neuron. This influx of sodium ions can depolarize the postsynaptic membrane if the synapse is excitatory.
  2. Calcium (Ca2+):
    • Neurotransmitter Release: Calcium ions are critical for triggering the fusion of synaptic vesicles with the presynaptic membrane. This process is essential for the release of neurotransmitters into the synaptic cleft.
    • Postsynaptic Response: In some cases, calcium ions can directly influence postsynaptic responses. For example, in certain types of synapses, calcium influx into the postsynaptic neuron can activate signaling pathways that contribute to synaptic plasticity or long-term changes in synaptic strength.

Overall, the exchange of sodium and calcium ions at the synapse is essential for both the transmission of signals from the presynaptic neuron to the postsynaptic neuron and for regulating synaptic function and plasticity. These ion movements are tightly regulated and coordinated to ensure precise and efficient neural communication in the nervous system.

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12
Q

What is the role of calcium at the nerve terminal

A

Exchange of sodium and calcium sends the action potential along the membrane of the nerve all the way to the nerve terminal when it gets there,it causes calcium gates to open and these calcium gates attach themselves to the membrane of the terminal and that is where the synaptic vesicles are exocytosed to the synaptic cleft. Exchange of sodium and calcium sends the action potential along the membrane of the nerve all the way to the nerve terminal when it gets there,it causes calcium gates to open and these calcium gates attach themselves to the membrane of the terminal and that is where the synaptic vesicles are exocytosed to the synaptic cleft. The neurotransmitters in the synaptic vesicles will decide whether they are going to propagate the action potential or they aren’t going to propagate the action potential.

Calcium is responsible for the synaptic vesicles that contain the neurotransmitters to be released to wherever it has to

Calcium is responsible for the synaptic vesicles that contain the neurotransmitters to be released to wherever it has to.

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13
Q

When does repolarization occur?
At what mV does it occur?

A

Repolarization occurs immediately after the peak of the action potential. Typically, the peak of the action potential is around +30 to +40 mV. Repolarization begins when the membrane potential reaches this peak and the voltage-gated sodium (Na⁺) channels inactivate while the voltage-gated potassium (K⁺) channels open.

  1. Peak of the Action Potential: Around +30 to +40 mV.
  2. Repolarization Starts: Immediately after the peak when the membrane potential is at +30 to +40 mV.

During repolarization, the membrane potential moves from the positive peak back towards the negative resting membrane potential (around -70 mV).

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14
Q

Explain the sodium equilibrium potential
Sodium is higher in which part of the cell? Extracellular or intracellular
What is the equilibrium potential for Na?

A

Sodium is higher in the Extracellular space and lower in intracellular space.

The concentration gradient for Na tends to move this ion into the cell because Na is higher outside and lower inside.
2 The inside of the cell becomes more positive as Na+ ions move to the inside down their concentration gradient.
3 The outside becomes more negative as Na ions move in, leaving behind in the ECF unbalanced negatively charged ions, mostly C. So they leave the ECf and move into the ICF
4 The resulting electrical gradient tends to move Na out of the cell.
5 No further net movement of Nat occurs when the outward electrical gradient exactly counterbalances the inward concentration gradient. The membrane potential at this equilibrium point is the equilibrium potential for Nat (ENa+) at +60 mV.

At the equilibrium potential, the movement of sodium ions into the cell (driven by both the concentration gradient and electrical gradient) is equal to the movement of sodium ions out of the cell.

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15
Q

What is equilibrium potential?

Action potential generation is based on the electrochemical gradient as well as movement of what two ions?

A

The equilibrium potential for an ion is the membrane potential at which there is no net flow of that particular ion in or out of the cell. It’s determined by the concentration gradient of the ion across the membrane and the ion’s charge. The most common ions of interest are sodium (Na⁺) and potassium (K⁺).

Action potential is based on movement of sodium and potassium across the cell membrane.

During depolarization, Na⁺ rushes into the cell due to its electrochemical gradient (high concentration outside and electrical attraction to the negative interior), causing the membrane potential to become positive.

During repolarization, K⁺ flows out of the cell due to its electrochemical gradient (high concentration inside and electrical repulsion from the now-positive interior), driving the membrane potential back towards a negative value.

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16
Q

Explain the potassium equilibrium potential
Potassium is higher in which part of the cell? Extracellular or intracellular
What is the equilibrium potential for K or at what mV is K at equilibrium ?(it’s in mV)

Development of the equilibrium potential for K+.
The membrane is permeable to K+ but not Cl. Explain how this is useful in creating equilibrium potential for K+

A

1
The concentration gradient for K+ tends to move this ion out of the cell.
The outside of the cell becomes more positive as K* ions move to the outside down their concentration gradient.
The membrane is impermeable to the large intracellular protein anion (A). The inside of the cell becomes more negative as K+ ions move out, leaving behind A-.
4
The resulting electrical gradient tends to move K+ into the cell.
5
No further net movement of K+ occurs when the inward electrical gradient exactly counterbalances the outward concentration gradient. The membrane potential at this equilibrium point is the equilibrium potential for K+ (Ek+) at
-90 mV.

When a membrane is permeable to K⁺ but not permeable to Cl⁻, and there is a concentration gradient of K⁺ across the membrane, the following process occurs, leading to the development of the equilibrium potential for K⁺:

  1. Initial Condition:
    • Inside the cell: High K⁺, High Cl⁻ (to balance charge)
    • Outside the cell: Low K⁺, Low Cl⁻

There is no net charge difference initially because positive and negative ions are balanced on both sides.

  1. Diffusion of K⁺:

Since the membrane is permeable only to K⁺, these ions begin to move down their concentration gradient, from inside to outside.

  1. Development of Charge Separation:

As K⁺ moves out:
• The inside becomes more negative because positive charges (K⁺) are leaving.
• The outside becomes more positive.

But Cl⁻ cannot follow to balance the charge because the membrane is not permeable to it.

  1. Opposing Electrical Gradient Builds Up:

The growing negative charge inside the membrane begins to attract K⁺ back and oppose further K⁺ efflux.

  1. Equilibrium Potential is Reached:

Eventually, the chemical driving force (concentration gradient) pushing K⁺ out is exactly balanced by the electrical force pulling K⁺ back in.

At this point, there is no net movement of K⁺, and the equilibrium potential for K⁺ (also called Eₖ) is established.

  1. Calculated by the Nernst Equation:


This gives the voltage across the membrane that balances the concentration gradient of K⁺.

Yes, Cl⁻ not being permeable actually helps the K⁺ equilibrium potential to develop and remain stable.

Here’s why:

  1. Fixed Negative Charges Inside:

When K⁺ leaves the cell, the inside becomes negatively charged.
If Cl⁻ could also leave, it would follow K⁺ (because opposite charges attract), and reduce the buildup of negative charge inside.
This would weaken the electrical force pulling K⁺ back in, so Eₖ would not develop properly.

  1. Membrane Selectivity Is Key:

The membrane’s impermeability to Cl⁻ means the negative charges remain inside as K⁺ leaves.
This amplifies the electrical gradient, helping the inside become more negative quickly, which opposes further K⁺ loss.

  1. Stable Equilibrium Potential:

With Cl⁻ unable to move, only K⁺ contributes to the charge separation.
This makes the equilibrium potential for K⁺ well-defined and predictable using the Nernst equation.

In summary:
Cl⁻ not being permeable supports and stabilizes the formation of the K⁺ equilibrium potential by allowing a strong, unopposed electrical gradient to build up.

Would you like a simple analogy to make this clearer?

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17
Q

Define the Nernst equation and what it determines

A

Used to calculate the equilibrium potential for an ion at a given concentration difference across the membrane (assuming membrane is permeable to ion). The Nernst equation is indeed used to calculate the equilibrium potential for a specific ion based on its concentration difference across the cell membrane. It helps determine the voltage at which there is no net flow of that ion across the membrane
Determines the electrical force required to just balance a given diffusion force ([ion]in - [ion]out).
cell

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18
Q

What is the calculation for the Nernst equation

Note: equilibrium potential for sodium is +65mV, for potassium is -90mV, for chloride is -70mV

A

Here’s the Nernst equation in detail:
Original equation is Eion =(RT/zF)In([ion]out/[ion]in)

Where R is universal gas constant,T is temperature in Kelvin,F is faraday constant

However, at body temperature (approximately 37°C or 310 K), the equation can be simplified and converted to a more convenient form for practical use in biological system. This simplified Nernst equation at body temperature is the equation below:

Eion = (60/z) log ( [ion]out/ [ion]in)

E ion = equilibrium potential for ion (mV)
z = ionic valence of ion (charge of the ion +/-) For example, for Na⁺, ( z = +1 ); for K⁺, ( z = +1 ); for Ca²⁺, ( z = +2 ); and for Cl⁻, ( z = -1 ).

[ion]out = extracellular concentration for ion (mmol/L)
[ion]in = intracellular concentration for ion (mmo/L)

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19
Q

Calculate electrochemical potential difference required to achieve electrochemical equilibrium for K+
• Eion = (60/z) log([ion]out / [ion]in)
E ion = equilibrium potential for ion
Z = ionic valence of ion
[ion]out= 5mM
[ion]in= 150 mM

What does your answer mean?

A

Ek+ = (60/+1) log(5 / 150)= -88.6 rounded to -89 mV
This means that when [K]in = 150 mM and [K]out = 5 mM, potassium flux is at
equilibrium when the cell is -89 mV inside.

Remember that equilibrium implies
that concentration force = electrical force; so that influx = efflux.

The chemical aspect of this equation is where the concentration gradient plays a role and the electrical aspect falls about the charges

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20
Q

The separation of charges across the cell membrane creates the membrane potential. Explain how this occurs
Which ions are concentrated more outside the cell than inside?
Which are more concentrated inside the cell than outside?

Why is the cell membrane selectively permeable to different ions?
Which ion mainly determines the resting membrane potential and why?
What is the Goldman-Hodgkin-katz equation and how is it different from the Nernst equation?
How is action potential generated ?

A

Separation of Charges

•	Ion Distribution: Cells maintain different concentrations of ions inside and outside the cell. Key ions include sodium (Na⁺), potassium (K⁺), chloride (Cl⁻), and various other anions (A⁻).
•	Na⁺: High outside, low inside
•	K⁺: High inside, low outside
•	Cl⁻: High outside, low inside
•	A⁻ (other anions, e.g., proteins): High inside, low outside
•	Selective Permeability: The cell membrane is selectively permeable to different ions, primarily due to specific ion channels that open and close in response to various signals.
•	Na⁺/K⁺ Pump: This pump actively transports 3 Na⁺ ions out of the cell and 2 K⁺ ions into the cell, using ATP. (So the pump sends the ions back to where they’re supposed to be. Which is sodium outside and potassium inside but the concentration gradient moves the ions to make things equal. )This creates and maintains the concentration gradients for Na⁺ and K⁺, contributing to the charge separation.
  1. Creation of Membrane Potential• Resting Membrane Potential: The membrane potential at rest, typically around -70 mV in neurons, is mainly determined by the K⁺ gradient. The cell membrane is more permeable to K⁺ than to Na⁺ or other ions at rest.
    • K⁺ tends to move out of the cell due to its concentration gradient(So because potassium on a regular is more inside, it wants to make things equal so it pumps
    Potassium out and sodium in. ), but this movement is balanced by the electrical gradient pulling K⁺ back in.
    • The equilibrium potential for K⁺ (Eₖ) is about -90 mV, which significantly influences the resting membrane potential.
    • Goldman-Hodgkin-Katz Equation: While the Nernst equation calculates the equilibrium potential for a single ion, the Goldman-Hodgkin-Katz equation considers multiple ions to determine the resting membrane potential:• ( V_m ) = membrane potential
    • ( P_{ion} ) = permeability of the ion
    • = concentration of the ion inside/outside the cell
  2. Action Potential Generation• Depolarization: A stimulus opens voltage-gated Na⁺ channels, allowing Na⁺ to rush into the cell. This influx of positive charge depolarizes the membrane, making the inside more positive.
    • Peak: The membrane potential can reach around +30 to +40 mV, where Na⁺ channels inactivate, and K⁺ channels open.
    • Repolarization: K⁺ ions flow out of the cell, restoring the negative membrane potential.
    • Hyperpolarization: The membrane potential briefly becomes more negative than the resting potential due to continued K⁺ efflux.
    • Return to Resting Potential: Na⁺/K⁺ pumps and leak channels restore the resting membrane potential.

Summary

•	Separation of Charges: Due to different ion concentrations inside and outside the cell and selective permeability of the membrane.
•	Membrane Potential: The electrical potential difference across the cell membrane due to this separation.
•	Resting Membrane Potential: Primarily determined by K⁺ gradients and membrane permeability.
•	Action Potential: A rapid change in membrane potential due to the sequential opening and closing of Na⁺ and K⁺ channels.
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21
Q

For action potential, There’s been a stimuli and the stimuli is great enough to destabilize the resting membrane potential to an extent that it reaches the threshold potential. What is the threshold potential?
How does it initiate action potential?

A

This is when the action potential fires. This causes depolarization. When the action potential is fired and it reaches the maximum,it goes back down or stabilizes. This is when repolarization starts(trying to send membrane back to its resting potential).

he threshold potential is the critical level to which the membrane potential must be depolarized in order to initiate an action potential. It is the point at which the influx of sodium ions (Na⁺) through voltage-gated sodium channels becomes self-sustaining, leading to a rapid and large depolarization of the membrane.

Key Points about Threshold Potential:

1.	Value: The threshold potential is typically around -55 mV in neurons, but this value can vary depending on the type of cell and its specific conditions.
2.	All-or-None Principle: If the membrane potential reaches the threshold, an action potential will be triggered. If the depolarization does not reach this threshold, an action potential will not occur. This is known as the “all-or-none” principle.

Initiation of Action Potential: The threshold potential marks the point where the membrane’s depolarization is sufficient to trigger the opening of enough voltage-gated Na⁺ channels to produce a rapid and irreversible depolarization. This leads to the peak of the action potential. If the depolarization is strong enough, it will bring the membrane potential to the threshold level (around -55 mV).
Action Potential Initiation: At threshold, voltage-gated Na⁺ channels open rapidly, causing a large influx of Na⁺. This depolarizes the membrane even further, triggering a full action potential.
5. Role in Excitability: The threshold potential is crucial in determining the excitability of a neuron. Factors that affect the threshold potential include:
• The density and distribution of voltage-gated Na⁺ channels.
• The presence of other ion channels and their conductance.
• The overall membrane properties, such as capacitance and resistance.

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22
Q

What is a neurotransmitter
State five properties of the neurotransmitter

Who discovered neuro transmitters
Neurotransmitters are classified by their chemical nature and functional nature. State them.

A

neurotransmitter is a chemical messenger that transmits signals across a synapse from one neuron (the presynaptic neuron) to another neuron, muscle cell, or gland cell (the postsynaptic cell).

A substance is generally considered a neurotransmitter if it is/has:
-synthesized in the neuron (typically in the cell body or in the synaptic terminals and stored in synaptic vesicles within the presynaptic neuron.
-found in the presynaptic terminal (must be present in the presynaptic terminal, where it is stored in synaptic vesicles ready for release.)
-released to have an effect in the postsynaptic cell (Upon arrival of an action potential at the presynaptic terminal, the neurotransmitter must be released into the synaptic cleft through a process called exocytosis and bind to specific receptors on the postsynaptic cell, eliciting a physiological response(effect could be excitatory or inhibitory))
-mimicked by exogenous application to the postsynaptic cell(When the neurotransmitter is applied externally (exogenously) to the postsynaptic cell, it should produce the same effect as when it is released endogenously from the presynaptic neuron. Example is Exogenous application of acetylcholine to the postsynaptic cell mimics the natural effects, such as muscle contraction when applied to a neuromuscular junction.)
-a specific mechanism for termination of its action.(This can include reuptake into the presynaptic neuron, enzymatic degradation, or diffusion away from the synaptic cleft.)

Neurotransmitters
• History-discovery by Loewi
• Inclusion criteria:
• Synthesized and released by neuron,
• Present in neuron,
• Neurotransmitters
• Classification: Chemical nature
• Amino acids: Involved in fast synaptic transmission. Excitatory or inhibitory eg:
GABA, glycine, glutamate, aspartate.
• Amines: Involved in slow synaptic transmission. Can be excitatory or inhibitory eg: adrenaline, noradrenaline, dopamine, serotonin, histamine.
• Others: Acetylcholine, NO…

Classification: functional
• Excitatory: opening of Na+ channels causing EPSP
• Inhibitory: opening of K+ channels causing IPSP

Here are examples of functionally classified synapses:

Excitatory Synapse (EPSP):
• Mechanism: Opening of Na⁺ channels, allowing Na⁺ to enter the postsynaptic neuron and make the membrane potential more positive (toward threshold).
• Example:
• Glutamate acting at AMPA receptors in the hippocampus or cortex.
• Acetylcholine at nicotinic receptors in the neuromuscular junction.

Excitatory neuro-
transmitters
1. Acetycholine
2. Nitric oxie
3. Histamine
4, Clutamale
5, Aspartae

Inhibitory Synapse (IPSP):
• Mechanism: Opening of K⁺ or Cl⁻ channels, causing the membrane potential to become more negative (hyperpolarized).
• Examples:
• GABA acting at GABA-A receptors (Cl⁻ channels) in the brain.
• Glycine acting in the spinal cord to open Cl⁻ channels.
• Some GABA-B receptors open K⁺ channels (inhibitory via K⁺ efflux).

Inhibitory neuro* transmitters
1. GABA
2. Glycine
3. Dopamine
4, Serotonin

Neurotransmitters with excitatory and inhibitory actions
1. Noradrenaline
2. Adrenaline

23
Q

. The neurotransmitters types are acetylcholine, biogenic amines, amino acids and neuropeptides.
Catecholamines are derived from what amino acid?
Indoleamines are derived from what amino acid?
State two excitatory amino acids
State two inhibitory amino acids
Endorphin is what type of neurotransmitter?
Oxytocin and Vasoactive Intestinal Peptide (VIP) are what types of neurotransmitters?
Histamine is what type of neurotransmitter

A

Neurotransmitters in the Body
1.• Acetylcholine (ACh)
2.• Biogenic Amines:
• Catecholamines; these are Derived from tyrosine.(• Dopamine,• Norepinephrine, • Epinephrine) Remember TyroCat
•Indoleamines: Derived from tryptophan(•Serotonin: Regulates mood, appetite, and sleep,Melatonin)
remember TryptoIndo
•Histamine: Involved in arousal, attention, and allergic responses.

3• Amino Acids:
• Excitatory Amino Acids(• Aspartate,Glutamate)
• Inhibitory Amino Acids:
(• Gamma-amino-butyric Acid (GABA), • Glycine)

4.• Neuropeptides:
• Endogenous opioids (for example, endorphin for pain regulation)
• Vasoactive Intestinal Peptide (VIP) which plays a role in vasodilation and relaxes smooth muscles in the GIT
• Oxytocin

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Q

At the synaptic cleft, the action potential causes release of calcium through voltage gated calcium channels. These channels open to allow calcium to enter. This causes binding of the vesicles that hold neurotransmitters and the membrane of the neuron. When they bind, the neurotransmitters are synapsed into the synaptic cleft then they go and bind to the receptors they are to go and bind to(the post synaptic receptors). Whether it produces an inhibitory or excitatory effect depends on the type of neurotransmitter. After doing its effect. It is either broken down to be recycled to produce more of it later or diffused out of the cleft or undergoes active neurotransmitter reuptake by presynaptic cell

Or The presynaptic neuron at rest. Calcium hannels are closed, and no neurotransmitter is being released. (b) An active presynaptic neuron. ommunication occurs as follows: The membrane is depolarized by the arrival of an action otential. 2 Calcium channels open. 3 Calcium enters the cell and triggers the release of eurotransmitter by exocytosis. Neurotransmitter diffuses across the synaptic cleft; some of it inds to receptors on the postsynaptic cell membrane. A response is produced in the ostsynaptic cell. 6 Some neurotransmitter is degraded by enzymes. Some neurotransmitter s taken up by the presynaptic cell.
® Some neurotransmitter (or products of its degradation)

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Glutamate is an excitatory neurotransmitter Which neurotransmitters are inhibitory How do they work as inhibitors ? Which ion is responsible for the hyper polarization that occurs in the two inhibitory neurotransmitters? Why?
GABA(Gamma-Aminobutyric Acid (GABA)) Glycine GABA(Gamma-Aminobutyric Acid (GABA)) Function: predominantly found in brain. Reduces neuronal excitability by increasing the permeability of the neuron membrane to chloride ions, leading to hyperpolarization. Hyperpolarizes neurons by allowing chloride ions to enter, making it less likely for the neuron to fire an action potential. • Receptors: GABA_A (ionotropic, fast-acting) and GABA_B (metabotropic, slower-acting). Glycine: • Location: Mainly in the spinal cord and brainstem. • Function: Acts as an inhibitory neurotransmitter by increasing chloride ion influx, which hyperpolarizes the neuron and inhibits action potential formation. Hyperpolarizes neurons in the spinal cord and brainstem, contributing to motor control and sensory signal processing. • Receptors: Glycine receptors (ionotropic). To determine whether repolarization is due to the influx of chloride ions or the efflux of potassium ions, consider the following: ### **1. Potassium Efflux (K+ leaving the cell):** - **Typical Mechanism:** Most commonly, repolarization occurs due to the **efflux of potassium ions (K+)**. When K+ ions leave the cell, they carry positive charges out of the cell, making the inside of the cell more negative and bringing the membrane potential back toward the resting level. - **Context:** This is the standard mechanism during the repolarization phase of an action potential. ### **2. Chloride Influx (Cl- entering the cell):** - **Alternative Mechanism:** In some cases, repolarization can also occur due to the **influx of chloride ions (Cl-)**. Since chloride ions are negatively charged, when they enter the cell, they increase the negativity inside the cell, contributing to repolarization. - **Context:** This mechanism is less common and typically occurs in specific situations, like when chloride channels are activated in certain types of neurons. ### **Key Differences:** - **Potassium Efflux** is the **default** and most common method of repolarization, associated with the normal process of returning the cell to its resting membrane potential after depolarization. - **Chloride Influx** can cause repolarization in **specific situations** where chloride channels are involved. ### **When to Use Which:** - **If the question mentions a typical repolarization event in a neuron following an action potential, it's likely due to potassium efflux.** - **If the question involves scenarios where chloride channels are specifically activated or involved, consider chloride influx.** So, if you encounter a question on repolarization in an MCQ: - **Default to potassium efflux** unless the context clearly indicates chloride influx . When discussing the mechanism of action of GABA and glycine, these neurotransmitters cause **hyperpolarization** by **increasing the permeability to chloride ions (Cl-)**. This is a key point to remember because: ### **GABA and Glycine Mechanism:** - **Hyperpolarization via Chloride Influx:** - GABA and glycine are inhibitory neurotransmitters. When they bind to their respective receptors on the postsynaptic neuron, they open chloride channels. - **Chloride ions (Cl-)** are negatively charged. When these ions enter the neuron, they make the inside of the cell more negative. - This increase in negativity inside the cell is what causes **hyperpolarization**, making it harder for the neuron to reach the threshold needed to fire an action potential. ### **Why It’s Different from Potassium Efflux:** - While **potassium efflux** (K+ leaving the cell) also leads to a more negative membrane potential (repolarization or hyperpolarization), **chloride influx** is particularly associated with **inhibitory** neurotransmission, which is crucial for the actions of GABA and glycine. ### **Key Takeaway:** - **GABA and glycine** cause **hyperpolarization** primarily through the **influx of chloride ions**, not potassium efflux. This influx increases the negative charge inside the neuron, making it less likely to fire, which is why they are classified as inhibitory neurotransmitters. When you see a question about GABA or glycine causing hyperpolarization: - **Remember:** It's due to **chloride influx**, which increases the cell's negative charge and inhibits action potential generation.
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Glutamate is an excitatory neurotransmitter How does it work and what are it’s receptors What is the difference between the two receptors Which of the receptors produces a long lasting effect
• Glutamate: • Receptors: NMDA, AMPA, kainate (ionotropic), and mGluRs (metabotropic). • Effect: Increases the likelihood of an action potential by allowing positively charged ions (like sodium and calcium) to enter the neuron, depolarizing it. 1. Kainate Receptors (Ionotropic): • Type: Ionotropic receptors, meaning they directly gate ion channels. • Activation: Activated by the neurotransmitter glutamate, specifically by kainic acid which is a structural analog of glutamate. • Function: Mediate fast excitatory neurotransmission. • Effect: When activated, they allow ions (usually sodium and potassium) to pass through, causing a rapid change in membrane potential, leading to neuronal excitation. • Subtypes: There are several subtypes (GluK1-5) which are involved in different neuronal functions. 2. Metabotropic Glutamate Receptors (mGluRs): • Type: Metabotropic receptors, meaning they are coupled to G-proteins and do not directly gate ion channels. • Activation: Also activated by glutamate, but they respond to different structural forms of glutamate compared to kainate receptors. • Function: Modulate synaptic transmission and neuronal excitability through second messenger systems. • Effect: When activated, they initiate signaling cascades inside the cell, leading to slower and longer-lasting effects compared to ionotropic receptors. • Subtypes: Divided into three groups (Group I, II, and III), each with multiple subtypes, influencing various aspects of neuronal function and plasticity. Summary: Kainate receptors are ionotropic, meaning they directly affect ion flow and are involved in rapid synaptic transmission. In contrast, mGluRs are metabotropic, signaling through second messengers to modulate neuronal activity and are involved in more nuanced and longer-lasting effects on synaptic transmission and neuronal function.
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**What happens to the membrane potential if the extracellular potassium concentration increases significantly?** - a) It becomes more negative. - b) It becomes more positive. - c) It remains unchanged. - d) It oscillates between positive and negative values. Which of the following events will lead to a more negative membrane potential (hyperpolarization)?** - a) Influx of sodium ions. - b) Efflux of potassium ions. - c) Influx of calcium ions. - d) Decreased membrane permeability to potassium ions.
In an MCQ setting, understanding the context of potassium ion movement (efflux or influx) is crucial for determining whether it leads to a more positive or negative membrane potential. Here are the specific contexts where you would choose each option: ### Potassium Efflux Leading to Negative Membrane Potential **Context: Resting Membrane Potential and Action Potential Phases** - **Resting Membrane Potential:** Potassium efflux through leak channels contributes to the negative resting membrane potential. - **Repolarization Phase:** During an action potential, potassium efflux through voltage-gated potassium channels helps restore the negative resting membrane potential after depolarization. - **Hyperpolarization:** Extended efflux of potassium after an action potential makes the inside of the cell even more negative than the resting potential. **Example MCQ:** **Which of the following events will lead to a more negative membrane potential (hyperpolarization)?** - a) Influx of sodium ions. - b) Efflux of potassium ions. - c) Influx of calcium ions. - d) Decreased membrane permeability to potassium ions. **Answer:** b) Efflux of potassium ions. ### Potassium Efflux Leading to Positive Membrane Potential **Context: General Cellular Context and Equilibrium Potential** - **Increased Extracellular Potassium:** In cases where the extracellular concentration of potassium is significantly increased, the reduced gradient decreases the potassium efflux, leading to a less negative (more positive) membrane potential compared to the normal resting state. **Example MCQ:** **What happens to the membrane potential if the extracellular potassium concentration increases significantly?** - a) It becomes more negative. - b) It becomes more positive. - c) It remains unchanged. - d) It oscillates between positive and negative values. **Answer:** b) It becomes more positive. So chat gpt said that normally, potassium is more inside right so it has the propensity to move out and make the inside more negative and it moves out solely because of the difference in concentration gradient. But once it moves and then potassium becomes more outside, it’ll be like it’s okay don’t move again. So less potassium will leave the cell cuz outside is already a lot. So it’ll make the inside more positive cuz potassium isn’t going out again and it’s staying inside. So for the normal, as potassium is more inside, it moves out to cause repolarization. But it doesn’t move out to become more than the conc inside. It just moves out to balance things and make the resting membrane potential come back to its original state which is negative. This is why the inside is negative ### Key Points to Remember 1. **Efflux of Potassium Ions (K⁺):** - Generally leads to a more negative membrane potential. - Relevant during repolarization and hyperpolarization phases of an action potential. 2. **Increased Extracellular Potassium:** - Reduces the potassium concentration gradient. - Leads to less efflux of K⁺, making the membrane potential less negative (more positive). ### Additional MCQ Questions **Question 20:** **During the repolarization phase of an action potential, the membrane potential becomes more negative due to:** - a) Influx of sodium ions. - b) Efflux of potassium ions. - c) Influx of calcium ions. - d) Influx of chloride ions. **Answer:** b) Efflux of potassium ions. **Question 21:** **If the extracellular potassium concentration decreases significantly, the membrane potential would:** - a) Become more negative. - b) Become more positive. - c) Remain unchanged. - d) Oscillate between positive and negative values. **Answer:** a) Become more negative (because a steeper gradient would increase K⁺ efflux). **Question 22:** **Which of the following conditions is most likely to lead to depolarization of the neuronal membrane?** - a) Increased efflux of potassium ions. - b) Decreased extracellular sodium concentration. - c) Increased influx of chloride ions. - d) Increased influx of sodium ions. **Answer:** d) Increased influx of sodium ions. **Question 23:** **Hyperpolarization is primarily caused by:** - a) Closing of sodium channels. - b) Influx of potassium ions. - c) Efflux of potassium ions. - d) Opening of sodium channels. **Answer:** c) Efflux of potassium ions. **Question 24:** **What is the primary reason for the negative resting membrane potential in neurons?** - a) Efflux of sodium ions. - b) Efflux of potassium ions. - c) Influx of calcium ions. - d) Influx of chloride ions. **Answer:** b) Efflux of potassium ions. These questions and explanations should help you understand the conditions under which potassium ion movements lead to changes in the membrane potential, aiding in the correct choice of answers in an MCQ setting.
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In which phase of mitosis would chromosomes line up at the centre of the spindle: A. anaphase B. interphase C. prophase D. metaphase In a cell cycle which phase takes the longest time to complete: A. anaphase B. interphase C. prophase D. telophase Which neurotransmitter do all motor neurons release at their synapses with skeletal muscle cells? A. ACh B. ATP C. GABA D. norepinephrine 4.Which one of the following parts of the nervous system carries impulses towards the brain? A. peripheral nervous system B. somatic nervous system C. autonomic nervous system D. parasympathetic division 5. What is the primary function of the cerebellum? A. it regulates such things as body temperature, water balance and emotional responses B. it refi nes/adjusts learned motor movements so that they are performed smoothly. C. it controls our automatic functions such as breathing, digestion and D. it is the origin of our conscious thoughts and intellectual functions 6. Which best describes a nerve? A. dendrites, cell bodies, axons, Schwann cells B. dendrites, cell bodies, axon hillock, axon terminals, vesicles C. dendrites, cell bodies, axon hillock, axon terminals, Schwann cells, D. axons, blood vessels, connective tissue, Schwann cells Cell membranes can maintain a difference in electrical charge between the interior of the cell and the extracellular fl uid. What is this charge difference called? A. excitability B. the membrane potential C. the action potential D. the sodium-potassium pump
1.D. Prometaphase is when chromosomes are in the process of attaching to spindle fibers and moving toward the center. • Metaphase is when they line up at the center. • Anaphase is when chromatids are pulled toward opposite poles. 2.B 3.A-The correct answer is: **A. ACh (Acetylcholine)** All motor neurons release acetylcholine (ACh) at their synapses with skeletal muscle cells, where it binds to receptors on the muscle cell membrane and triggers muscle contraction. Acetylcholine (ACh) is a versatile neurotransmitter that plays several critical roles in both the central nervous system (CNS) and the peripheral nervous system (PNS). Here are some of its key functions: ### 1. **Muscle Contraction (Peripheral Nervous System)** - **Neuromuscular Junction:** ACh is the primary neurotransmitter at the neuromuscular junction, where it binds to receptors on skeletal muscle cells, causing them to contract. - **Autonomic Nervous System:** ACh is involved in both the sympathetic and parasympathetic branches of the autonomic nervous system. - **Parasympathetic System:** ACh is the main neurotransmitter that activates the "rest and digest" responses, such as slowing the heart rate, increasing digestion, and promoting relaxation. - **Sympathetic System:** In the sympathetic system, ACh is released by preganglionic neurons and then relayed by norepinephrine or epinephrine in the postganglionic neurons. ### 2. **Cognitive Functions (Central Nervous System)** - **Memory and Learning:** In the brain, ACh is important for memory formation, learning, and attention. It is particularly active in the hippocampus, a region associated with memory. - **Arousal and Sleep:** ACh plays a role in promoting wakefulness and alertness. It is also involved in the regulation of REM sleep. ### 3. **Modulation of Heart Rate** - In the heart, ACh released by the vagus nerve slows the heart rate by acting on muscarinic receptors in the cardiac muscle, promoting relaxation and decreasing the rate of contractions. ### 4. **Regulation of Secretions** - **Exocrine Glands:** ACh stimulates the secretion of saliva, sweat, and other digestive juices by acting on glands. - **Gastrointestinal Tract:** ACh increases peristalsis and secretion in the gastrointestinal tract, aiding in digestion. ### 5. **Inhibition in Certain Contexts** - **Muscarinic Receptors:** When ACh binds to muscarinic receptors in certain smooth muscles (like those in the lungs), it can cause contraction, leading to bronchoconstriction. However, in other contexts, it can cause relaxation of smooth muscles, such as in blood vessels. ### 6. **Autonomic Reflexes** - ACh is involved in various autonomic reflexes, such as the baroreceptor reflex, which helps maintain blood pressure homeostasis. In summary, acetylcholine is involved in a wide range of functions, from stimulating muscle contractions to modulating cognitive processes and autonomic functions. Its effects vary depending on the type of receptor it binds to (nicotinic or muscarinic) and the location of these receptors in the body. Mmm 4.A-Yes, the somatic nervous system does include the motor system, which controls voluntary muscle movements. However, when considering the question about which part of the nervous system carries impulses toward the brain, it's important to focus on the direction of the nerve impulses. ### Explanation: - **Afferent (Sensory) Pathways:** These pathways carry sensory information **towards** the brain and spinal cord. They are part of the **peripheral nervous system** (PNS), which includes all nerves outside the brain and spinal cord. - **Efferent (Motor) Pathways:** These pathways carry impulses **away from** the brain and spinal cord to muscles and glands. The somatic nervous system primarily consists of these efferent pathways, especially when dealing with voluntary muscle control. ### Answer Analysis: - **A. Peripheral Nervous System (PNS):** The PNS includes both afferent (sensory) and efferent (motor) nerves. The sensory (afferent) nerves carry impulses towards the brain, making this the correct answer. - **B. Somatic Nervous System:** While the somatic nervous system includes both sensory (afferent) and motor (efferent) components, it is better known for controlling voluntary movements through its motor functions. It does carry some sensory impulses to the brain, but the PNS as a whole is a broader and more accurate answer. - **C. Autonomic Nervous System (ANS):** This system controls involuntary functions like heart rate and digestion. It includes both afferent and efferent nerves, but it primarily deals with involuntary processes. - **D. Parasympathetic Division:** This is a part of the autonomic nervous system that controls "rest and digest" functions. It primarily sends efferent impulses from the brain to various organs, rather than carrying sensory information to the brain. ### Conclusion: The correct answer is **A. Peripheral Nervous System** because it encompasses the afferent nerves that carry sensory information toward the brain. The somatic nervous system is involved in this process, but the PNS more accurately represents the overall function described in the question. To decide between choosing the **Peripheral Nervous System (PNS)** or the **Somatic Nervous System (SNS)** in a multiple-choice question, focus on the specific context of the question: ### **1. Peripheral Nervous System (PNS)** - **When to Pick PNS:** - The question refers to the broad category of nerves outside the brain and spinal cord, including both sensory and motor functions. - The question is about general sensory information being carried to the brain. - The question addresses both autonomic (involuntary) and somatic (voluntary) functions, or doesn’t specify between them. - Example: "Which part of the nervous system includes sensory pathways that carry information to the brain?" ### **2. Somatic Nervous System (SNS)** - **When to Pick SNS:** - The question focuses specifically on **voluntary** control, like movement of skeletal muscles. - The question refers to motor functions or reflex arcs that involve skeletal muscles. - The question is about conscious control, like responding to stimuli with movement. - Example: "Which part of the nervous system controls voluntary movements of skeletal muscles?" ### **Key Differences:** - **PNS** is the umbrella term that includes both the SNS and the Autonomic Nervous System (ANS). It refers to all nerves outside the central nervous system, covering both sensory (afferent) and motor (efferent) pathways. - **SNS** is a subdivision of the PNS specifically responsible for voluntary movements and the reflex arcs involving skeletal muscles. ### **Practical Tips:** - **For Sensory Input:** If the question involves sensory input (like touch, pain, or temperature) being transmitted to the brain, **PNS** is usually the correct answer. - **For Motor Output:** If the question involves voluntary muscle control or motor output, **SNS** is usually the correct answer. - **General Context:** If the question is general and doesn't specify whether it's talking about sensory or motor functions, **PNS** is often the safer choice. By keeping these distinctions in mind, you can better identify when to pick PNS or SNS based on the context of the question. 5. The correct answer is: **B. it refines/adjusts learned motor movements so that they are performed smoothly.** ### Explanation: - **Cerebellum**: The cerebellum is primarily responsible for coordinating voluntary movements, ensuring that these movements are smooth and accurate. It refines and adjusts learned motor activities such as walking, running, or playing a musical instrument. This function helps in maintaining balance, posture, and fine-tuning motor actions. ### Other Options: - **A. it regulates such things as body temperature, water balance, and emotional responses**: This describes the functions of the **hypothalamus**. - **C. it controls our automatic functions such as breathing, digestion**: This describes the functions of the **medulla oblongata** and other parts of the brainstem, not the cerebellum. The correct answer is still: **B. it refines/adjusts learned motor movements so that they are performed smoothly.** ### Explanation of the New Option: - **D. it is the origin of our conscious thoughts and intellectual functions**: This describes the function of the **cerebrum** or **cerebral cortex**, not the cerebellum. The cerebrum is involved in higher brain functions like thinking, reasoning, consciousness, and voluntary motor functions. So, the cerebellum's primary role remains in refining and coordinating learned motor movements, making option B the correct answer. 6. **D. axons, blood vessels, connective tissue, Schwann cells** is the correct answer. ### Explanation: - A **nerve** is a bundle of axons, which are long extensions of neurons. - Nerves also contain **blood vessels** to supply nutrients and remove waste. - **Connective tissue** surrounds and protects the nerve fibers, providing structural support. - **Schwann cells** are glial cells that wrap around the axons in the peripheral nervous system, forming the myelin sheath, which insulates the axons and speeds up nerve impulse transmission. This option best describes the structure of a nerve, which consists of multiple axons bundled together, supported by connective tissue, with associated blood vessels and Schwann cells. Option **B** is incorrect because it describes the components of a single neuron, not a nerve. ### Here's the breakdown: - **Dendrites, cell bodies, axon hillock, axon terminals, vesicles** are all parts of a single neuron. - **Dendrites** receive incoming signals. - **Cell bodies** (soma) contain the nucleus and other organelles. - The **axon hillock** is where the action potential is initiated. - **Axon terminals** are the endpoints of the axon where neurotransmitters are released. - **Vesicles** contain neurotransmitters within the axon terminals. ### Why This Doesn’t Describe a Nerve: - A **nerve** is not just one neuron but a bundle of many axons (from multiple neurons) along with blood vessels, connective tissue, and Schwann cells. - Option B describes the structural components of an individual neuron rather than the collective structure of a nerve, which includes multiple axons bundled together and supported by other tissues and cells like Schwann cells. Therefore, **D** is the correct answer because it accurately describes the collective structure of a nerve, while **B** only describes a single neuron’s components. 7. The correct answer is: **B. the membrane potential** ### Explanation: - **Membrane Potential**: This is the difference in electrical charge between the interior of the cell and the extracellular fluid. It is crucial for the function of neurons and muscle cells, as it creates the conditions necessary for the generation and transmission of electrical signals. ### Other Options: - **A. excitability**: Refers to the ability of a cell to respond to stimuli and generate action potentials. - **C. the action potential**: Is the rapid rise and fall in membrane potential that occurs when a cell is stimulated. - **D. the sodium-potassium pump**: Is a mechanism that helps maintain the membrane potential by actively transporting sodium out of the cell and potassium into the cell.
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The percentages of water in each of the fluid compartments are approximately ______ intracellular fluid, ______ interstitial fluid and ______ plasma A 22%, 13%, 65% B 70%, 20%, 10% C 65%, 22%, 13% D 20%, 10%, 70% How many kg makes 1litre? For a 70kg person,how much litres of water is in the ICF?
Answer is C. The percentages I initially mentioned (65%, 22%, 13%) are based on **total body water**. The ones you referenced (40%, 16%, 4%) are based on **total body weight**. Here’s a breakdown of how they relate to each other: ### **Based on Total Body Water:** - **Intracellular Fluid (ICF)**: ~**65%** of total body water. - **Extracellular Fluid (ECF)**: ~**35%** of total body water. - **Interstitial Fluid**: ~**22%** of total body water. - **Plasma**: ~**13%** of total body water. ### **Based on Total Body Weight:** - **Intracellular Fluid (ICF)**: ~**40%** of body weight. - **Extracellular Fluid (ECF)**: ~**20%** of body weight. - **Interstitial Fluid**: ~**16%** of body weight. - **Plasma**: ~**4%** of body weight. ### **How They Differ:** - **Total Body Water Distribution**: - Refers to how water is distributed across different compartments (ICF, interstitial fluid, and plasma). - It typically shows the relative proportions of water within each compartment. - **ICF** holds a larger proportion of the body's water, so it's about 65% of the total body water. - **ECF** is divided between the interstitial fluid and plasma, making up the remaining 35% of total body water. - **Total Body Weight Distribution**: - Refers to how much of your body weight is made up by these fluids. - Since about 60% of your body weight is water, the ICF makes up about 40% of your total body weight, and the ECF makes up about 20%. - **ICF** accounts for 40% of your body weight, with ECF (interstitial fluid + plasma) making up the other 20%. ### Summary: - **Total Body Water** percentages show how water is divided across compartments. - **Total Body Weight** percentages show how much each fluid compartment contributes to your overall body weight. Understanding these differences helps in clinical contexts where knowing fluid distribution relative to either total body water or body weight is crucial, such as in dehydration or fluid overload situations. The total body water percentages are derived from the way water is distributed within the body's fluid compartments. Let's break down how these percentages are obtained: ### 1. **Understanding Total Body Water (TBW)** - **Total Body Water (TBW)** accounts for about **60% of a person’s body weight**. - This TBW is divided into two main compartments: - **Intracellular Fluid (ICF)**: Fluid inside cells. - **Extracellular Fluid (ECF)**: Fluid outside cells, which includes interstitial fluid (fluid between cells) and plasma (the liquid part of blood). ### 2. **Intracellular Fluid (ICF)** - **ICF** makes up about **two-thirds of the total body water**. - So, if TBW is 60% of body weight, then: - **ICF = 2/3 of 60% = 40% of body weight**. - **ICF = 2/3 of 100% of TBW = 65% of TBW**. ### 3. **Extracellular Fluid (ECF)** - **ECF** makes up about **one-third of the total body water**. - The ECF is further divided into: - **Interstitial Fluid** (between cells): About **3/4 of the ECF**. - **Plasma** (in blood vessels): About **1/4 of the ECF**. - So, if TBW is 60% of body weight, then: - **ECF = 1/3 of 60% = 20% of body weight**. - **ECF = 1/3 of 100% of TBW = 35% of TBW**. ### 4. **Breaking Down the ECF Further** - **Interstitial Fluid**: - 3/4 of the ECF is interstitial fluid. - **Interstitial Fluid = 3/4 of 20% = 15% of body weight**. - **Interstitial Fluid = 3/4 of 35% of TBW = ~22% of TBW**. - **Plasma**: - 1/4 of the ECF is plasma. - **Plasma = 1/4 of 20% = 5% of body weight**. - **Plasma = 1/4 of 35% of TBW = ~13% of TBW**. ### **Summary of TBW Percentages**: - **ICF**: ~65% of Total Body Water (TBW) - **ECF**: ~35% of Total Body Water (TBW) - **Interstitial Fluid**: ~22% of TBW - **Plasma**: ~13% of TBW Yes, that’s correct! Total body water (TBW) is typically estimated to be about 60% of total body weight in a healthy adult. Here’s a breakdown of that figure: • Total Body Water (TBW): Approximately 60% of body weight. • Intracellular Fluid (ICF): About 40% of body weight (approximately 65% of TBW). • Extracellular Fluid (ECF): About 20% of body weight (approximately 35% of TBW). • Interstitial Fluid: Approximately 16% of body weight (about 22% of TBW). • Plasma: Approximately 4% of body weight (about 13% of TBW Yes, the percentages are typically based on a **70 kg** person. Here's how to apply those percentages to individuals of different weights: 1. **For a 70 kg person**: - Total Body Water (TBW) = 60% of 70 kg = **42 kg** (or about **42 liters**, since 1 kg of water is approximately 1 liter). - Intracellular Fluid (ICF) = 40% of 70 kg = **28 kg** (or about **28 liters**). - Extracellular Fluid (ECF) = 20% of 70 kg = **14 kg** (or about **14 liters**). - Interstitial Fluid = 16% of 70 kg = **11.2 kg** (or about **11.2 liters**). - Plasma = 4% of 70 kg = **2.8 kg** (or about **2.8 liters**). 2. **For an 80 kg person**: - Total Body Water (TBW) = 60% of 80 kg = **48 kg** (or about **48 liters**). - Intracellular Fluid (ICF) = 40% of 80 kg = **32 kg** (or about **32 liters**). - Extracellular Fluid (ECF) = 20% of 80 kg = **16 kg** (or about **16 liters**). - Interstitial Fluid = 16% of 80 kg = **12.8 kg** (or about **12.8 liters**). - Plasma = 4% of 80 kg = **3.2 kg** (or about **3.2 liters**). 3. **For a 60 kg person**: - Total Body Water (TBW) = 60% of 60 kg = **36 kg** (or about **36 liters**). - Intracellular Fluid (ICF) = 40% of 60 kg = **24 kg** (or about **24 liters**). - Extracellular Fluid (ECF) = 20% of 60 kg = **12 kg** (or about **12 liters**). - Interstitial Fluid = 16% of 60 kg = **9.6 kg** (or about **9.6 liters**). - Plasma = 4% of 60 kg = **2.4 kg** (or about **2.4 liters**). ### Summary: - The **total body water** and its distribution between **ICF** and **ECF** can be calculated using the same percentage values, adjusted for the individual's body weight.
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Which of the following types of glutamate receptors is most closely associated with excitatory neurotransmission and is responsible for fast synaptic transmission? A) NMDA (N-methyl-D-aspartate) receptor B) AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor C) Kainate receptor D) Metabotropic glutamate recep
Answer is B The type of glutamate receptor most closely associated with excitatory neurotransmission and responsible for fast synaptic transmission is: B) AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor You would pick kainate receptors in MCQ questions where the focus is on: 1. **Excitatory neurotransmission, but not specifically fast transmission**: Kainate receptors are involved in excitatory signaling but are not as central to fast synaptic transmission as AMPA receptors. 2. **Specific roles of kainate receptors**: Questions about the role of kainate receptors in synaptic plasticity, modulation of neurotransmitter release, or less common excitatory pathways might be appropriate for selecting kainate. ### Example MCQ Where Kainate Would Be the Answer **Which of the following types of glutamate receptors is primarily involved in modulating synaptic transmission and may contribute to excitatory signaling in specific neural pathways?** - a) AMPA receptor - b) NMDA receptor - c) Kainate receptor - d) Metabotropic glutamate receptor **Answer:** c) Kainate receptor ### Explanation - **Kainate Receptors**: Involved in excitatory neurotransmission and can modulate the release of other neurotransmitters, but they are less commonly associated with the rapid, primary excitatory transmission that AMPA receptors mediate. - **AMPA Receptors**: Known for fast excitatory synaptic transmission. - **NMDA Receptors**: Involved in longer-term changes in synaptic strength and plasticity. - **Metabotropic Glutamate Receptors (mGluRs)**: Modulate neuronal activity through second messenger systems.
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The Nernst potential (also called equilibrium potential) is positive for: A. Na and Cl B. Na and K C. Na and Ca D. K and Cl
Answer is C The Nernst potential (or equilibrium potential) is positive for: **C. Na and Ca** ### Explanation: - **Sodium (Na)**: The equilibrium potential for sodium is positive because sodium ions are typically at higher concentrations outside the cell compared to inside. When sodium channels open, sodium ions move into the cell, which makes the inside of the cell more positive. - **Calcium (Ca)**: The equilibrium potential for calcium is also positive for similar reasons; calcium ions are at much higher concentrations outside the cell. When calcium channels open, calcium ions move into the cell, making the inside more positive. ### For Comparison: - **Potassium (K)**: The equilibrium potential for potassium is negative because potassium ions are at higher concentrations inside the cell. When potassium channels open, potassium ions move out of the cell, making the inside of the cell more negative. - **Chloride (Cl)**: The equilibrium potential for chloride can be negative or positive depending on the cell type and chloride concentrations, but it is often close to the resting membrane potential, which is typically negative. Thus, sodium and calcium both have positive Nernst potentials. The Nernst potentials (equilibrium potentials) for ions are determined using the Nernst equation. Here are the typical values for each ion: 1. **Sodium (Na⁺):** - **Equilibrium Potential**: Approximately +60 mV - This value can vary depending on the specific concentration gradients and conditions, but +60 mV is a common approximation for sodium in many neurons. 2. **Calcium (Ca²⁺):** - **Equilibrium Potential**: Approximately +120 mV - Calcium has a higher equilibrium potential compared to sodium due to its much higher extracellular concentration. 3. **Potassium (K⁺):** - **Equilibrium Potential**: Approximately -90 mV - Potassium's equilibrium potential is negative because potassium is more concentrated inside the cell and moves out, making the inside more negative. 4. **Chloride (Cl⁻):** - **Equilibrium Potential**: Typically around -65 mV - The equilibrium potential for chloride varies depending on the specific cell type and the relative concentrations of chloride inside and outside the cell.
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Which of the following terms describes synapses? a. Axodendritic b. Axosomatic c. Axoaxonic d. all of the above Neurotransmitters are released from the A. Collaterals B. Hillock C. Synapse D. Telodendria E. Synaptic knobs Substrate accumulation against its electrochemical gradient is by: a. Ion channel b. Facilitated diffusion c. Active transport d. Symport e. Antiport study of the functions of specific organ is A. System physiology B. Special physiology C. Histophysiology D. Cell physiology E. Histology
Here’s a more detailed explanation for each question: 1. **Which of the following terms describes synapses?** - **d. all of the above** - **Axodendritic**: This type of synapse occurs between the axon terminal of one neuron and the dendrite of another neuron. It is the most common type of synapse in the brain. - **Axosomatic**: This synapse is between the axon terminal of one neuron and the soma (cell body) of another neuron. It can have a significant impact on the neuron’s overall excitability. - **Axoaxonic**: This type of synapse occurs between the axon terminal of one neuron and the axon terminal of another neuron. It can modulate the release of neurotransmitters from the second neuron. - All these types are different configurations of synapses, hence "all of the above" is the correct answer. You're right that synapses can be broadly classified into **chemical** and **electrical** types. However, within chemical synapses, there are different structural types based on where the synapse occurs on the neuron. Here’s a breakdown: 1. **Chemical Synapses**: - **Chemical Synapses** use neurotransmitters to transmit signals from one neuron to another. These are the most common type of synapse. - They can be further categorized based on their anatomical locations: - **Axodendritic**: Synapse between the axon terminal of one neuron and the dendrite of another neuron. - **Axosomatic**: Synapse between the axon terminal and the soma (cell body) of another neuron. - **Axoaxonic**: Synapse between the axon terminal of one neuron and the axon terminal of another neuron. 2. **Electrical Synapses**: - **Electrical Synapses** use gap junctions to allow direct electrical communication between neurons. This type of synapse allows for very rapid signal transmission. - They are less common but are important for certain types of synchronized activity between neurons. **Summary**: - **Chemical Synapses**: Use neurotransmitters and can be categorized by their anatomical connections (axodendritic, axosomatic, axoaxonic). - **Electrical Synapses**: Use direct electrical connections (gap junctions) for rapid signaling. So, while the broad categories are chemical and electrical, there are specific structural types within the chemical synapse category. 2. **Neurotransmitters are released from the:** - **E. Synaptic knobs** - **Synaptic knobs** (or synaptic terminals) are the specialized structures at the end of an axon where neurotransmitters are stored in vesicles. When an action potential reaches the synaptic knob, it triggers the release of neurotransmitters into the synaptic cleft. 3. **Substrate accumulation against its electrochemical gradient is by:** - **c. Active transport** - **Active transport** is a process that uses energy (usually from ATP) to move substances against their concentration gradient. This is necessary for maintaining concentration differences across cell membranes, such as transporting ions or nutrients into cells when their concentrations are higher inside the cell than outside. **Symport** is a type of **active transport** where two substances are moved across the cell membrane in the same direction simultaneously. However, it typically involves moving one substance down its concentration gradient to drive the transport of another substance against its gradient. Here's why **symport** isn't the correct answer for substrate accumulation against its electrochemical gradient: 1. **Active Transport**: This is the general term for any process that requires energy (usually from ATP) to move substances against their electrochemical gradients. It includes both symport and antiport mechanisms. 2. **Symport**: Specifically refers to a type of active transport where two substances are transported in the same direction. While it does involve moving one substance against its gradient, the term symport itself doesn’t fully describe the broader concept of accumulating substrates against their gradient. 3. **Example of Symport**: The sodium-glucose transport protein (SGLT) in the intestines uses the sodium gradient (which is established by the Na⁺/K⁺ pump) to bring glucose into the cells against its gradient. In the context of your question, **active transport** is a more comprehensive term that encompasses all mechanisms, including symport and antiport, that move substances against their gradients. 4. **Study of the functions of a specific organ is:** - **B. Special physiology** - **Special physiology** (or systemic physiology) focuses on the specific functions and processes of individual organs and systems within the body. It looks at how organs work in isolation and how they contribute to the overall function of the organism. This contrasts with other types of physiology such as cell physiology (which focuses on cellular functions) or systemic physiology (which studies entire systems like the cardiovascular or respiratory system). Sure, here are some additional types of physiology beyond **special physiology**: 1. **Cell Physiology**: - Focuses on the functions and processes of individual cells, including how they interact with their environment and maintain homeostasis. 2. **Systemic Physiology**: - Studies the functions of organ systems as a whole, such as the cardiovascular system, respiratory system, or digestive system. 3. **Integrative Physiology**: - Examines how different organ systems work together to maintain homeostasis and overall function in the body. 4. **Comparative Physiology**: - Compares physiological processes across different species to understand how different organisms adapt to their environments. 5. **Pathophysiology**: - Looks at how physiological processes are altered in disease states, helping to understand the mechanisms behind various health conditions. 6. **Exercise Physiology**: - Studies the physiological responses and adaptations to physical exercise, including how exercise impacts different systems in the body. 7. **Developmental Physiology**: - Focuses on how physiological processes change from conception through aging, including growth, development, and aging. 8. **Environmental Physiology**: - Investigates how environmental factors, such as temperature, altitude, and nutrition, affect physiological processes and adaptation. 9. **Neurophysiology**: - Studies the physiology of the nervous system, including how neurons communicate and how the brain and spinal cord function. These subfields help in understanding various aspects of how organisms function, adapt, and respond to internal and external changes.
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On average total body water in a person is about 60% of their body weight. From the total body water, 2/3 of that, or 40% of body weight is intracellular fluid. The other 1/3 or 20% of body weight is extracellular fluid.
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Here's a breakdown of fluid compartments using the fractions you've mentioned: 1. **Total Body Water (TBW)**: - **Intracellular Fluid (ICF)**: \( \frac{2}{3} \) (or approximately 66%) of TBW. - **Extracellular Fluid (ECF)**: \( \frac{1}{3} \) (or approximately 33%) of TBW. 2. **Extracellular Fluid (ECF)**: - **Interstitial Fluid**: \( \frac{3}{4} \) (or approximately 75%) of ECF. - **Plasma Water**: \( \frac{1}{4} \) (or approximately 25%) of ECF. 3. **Fluid in the compartments**: - **Intracellular Fluid (ICF)**: \( \frac{2}{3} \) of TBW. - **Extracellular Fluid (ECF)**: \( \frac{1}{3} \) of TBW. - **Interstitial Fluid**: \( \frac{3}{4} \) of ECF. - **Plasma Water**: \( \frac{1}{4} \) of ECF. 4. **Specific Fractions of TBW**: - **Interstitial Fluid**: \( \frac{1}{4} \) of TBW (25%). - **Plasma Water**: \( \frac{1}{12} \) of TBW (approximately 8-10%). To summarize: - **ICF** makes up \( \frac{2}{3} \) of TBW. - **ECF** makes up \( \frac{1}{3} \) of TBW, which is further divided into: - **Interstitial Fluid**: \( \frac{3}{4} \) of ECF, or \( \frac{1}{4} \) of TBW. - **Plasma Water**: \( \frac{1}{4} \) of ECF, or \( \frac{1}{12} \) of TBW. These fractions help illustrate how body fluids are distributed across different compartments.
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Functional anatomy of a synapse. (a) The presynaptic neuron at rest. Calcium hannels are closed, and no neurotransmitter is being released. (b) An active presynaptic neuron. Communication occurs as follows: • The membrane is depolarized by the arrival of an action otential. 2 Calcium channels open. 3) Calcium enters the cell and triggers the release of eurotransmitter by exocytosis. • Neurotransmitter diffuses across the synaptic cleft; some of it inds to receptors on the postsynaptic cell membrane. E) A response is produced in the ostsynaptic cell. © Some neurotransmitter is degraded by enzymes. • Some neurotransmitter staken up by the presynaptic cell. ® Some neurotransmitter (or products of its degradation)
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Explain equilibrium potential under types of diffusion potential Note: In this type, chemical and electrical gradients are equal and opposite in direction. Explain these two statements under equilibrium potential: 1.It is Determined by a given set of ion conc. 2.The Magnitude of potential is directly proportional to magnitude of conc. gradient
It is the membrane potential at which there is no net movement of a specific ion. It reflects the balance between that ion’s concentration gradient and electrical gradient. The point where an ion stops moving in or out. Balance between charge and concentration. Net flux is 0. Influx = efflux Refers to electrical potential difference(voltage) or the diffusion potential that opposes or balances the tendency for diffusion down the concentration gradient. So this diffusion potential opposes or balances them so that they won’t move or diffuse down the concentration gradient. • No net mvt. of ions at equilibrium • Determined by a given set of ion conc. • Magnitude of potential directly proportional to magnitude of conc. gradient This statement is referring to equilibrium potential, which is the electrical potential difference (voltage) across a membrane that exactly balances the concentration gradient of a particular ion—so that there is no net movement of that ion across the membrane. Let’s break it down: “Determined by a given set of ion concentrations” • The equilibrium potential for an ion (like K⁺ or Na⁺) is calculated using the Nernst equation, which takes into account the concentration of that ion inside and outside the cell. • So, the value of the equilibrium potential depends entirely on these concentrations. “Magnitude of potential directly proportional to magnitude of concentration gradient” • A bigger difference in concentration between the inside and outside of the cell means a bigger electrical force is needed to balance it (i.e., a larger equilibrium potential). • This means that as the concentration gradient increases, the equilibrium potential becomes more positive or more negative, depending on the direction of the gradient and the charge of the ion. Example using Potassium (K⁺): • If inside = 140 mM, outside = 5 mM → steep gradient → large negative equilibrium potential (~ -90 mV). • If inside = 140 mM, outside = 70 mM → smaller gradient → less negative equilibrium potential (~ -61 mV). Would you like a short explanation of the Nernst equation next? Simple explanation Equilibrium potential is like the “balancing point” for an ion. It depends on how much of the ion is inside and outside the cell. • If there’s a big difference (like a lot more outside than inside), the cell needs a stronger electrical force to keep the ion from moving. • So, the bigger the difference in concentration(this is concentration gradient) , the bigger the equilibrium potential (either more positive or more negative).
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What type of diffusion potential refers to the difference that exists across the membrane of excitable cells at steady state? What’s the difference between excitable cells and non excitable cells and give three examples each Explain orthograde and retrograde transport in nerves State two motor proteins and their functions in transport of nerves.
Resting Membrane Potential: It refers to the difference that exists across the membrane of excitable cells at steady state. Note: All living cells have some resting membrane potential (RMP) • There is a constant RMP in cells of non-excitable tissues. 1. Resting Membrane Potential (RMP): • All living cells have a resting membrane potential—a small voltage difference across their membrane (usually -70 mV inside). • This is due to ion concentration differences (mainly K⁺, Na⁺, Cl⁻) and selective membrane permeability, mostly to K⁺. 2. Non-Excitable vs. Excitable Cells: • Non-excitable cells (e.g., skin, liver cells): Non-Excitable Cells(Have RMP but don’t generate action potentials)1. Epithelial cells – line organs and skin. 2. Liver cells (hepatocytes) – involved in metabolism and detox. 3. Fibroblasts – produce connective tissue. 4. Red blood cells (RBCs) – carry oxygen (no nucleus). 5. Endothelial cells – line blood vessels. 6. Adipocytes – fat storage cells. 7.Bone cells (osteocytes). 8. Immune cells – like macrophages or lymphocytes (some may become excitable under certain conditions, but generally not) • Have a constant RMP. • Don’t use electrical signals for communication. • Excitable cells (e.g., nerve, all types of muscle cells, pancreatic beta cells, sensory receptor cells like those in the eyes ear or skin.): • Have a resting membrane potential, but it can change quickly. • This change is called an action potential—used for electrical signaling. 3. Excitable Cells Examples: Cell Type Function of Excitability Nerve cells Transmit electrical signals (impulses). Muscle cells Contract in response to electrical signals. Pancreatic beta cells Release insulin when stimulated by glucose. So, “excitable” means they respond to stimuli by changing their RMP and using that to do something important. Note: Neurons in the brain are excitable. • Other brain cells (glial cells) are non-excitable. 4. Orthograde (Anterograde) vs. Retrograde Transport in Neurons: Neurons have long axons, and substances need to move up and down: • Anterograde transport = from cell body to axon terminal (forward) • Carries things like neurotransmitters, enzymes, organelles. • Done by a motor protein called kinesin. • Retrograde transport = from axon terminal back to cell body • Carries old materials, waste, or signals (like viruses or growth factors). • Done by dynein. 5. Kinesin and Dynein (Motor Proteins): Protein Direction Transport Type Kinesin Anterograde Outward (to axon terminal) Dynein Retrograde Inward (to cell body) These proteins “walk” along microtubules carrying cargo like tiny delivery trucks. So imagine the cell body is the house and you’re going back inside your house. That’s retrograde. And if you’re going to your house, you’re going to rest and unwind and eat and bring out waste materials and all. But if you’re going out, you’re going to work and all and that’s anterograde or orthograde. We have fast and slow anterograde transport: Yes, exactly! The neuron sends some materials slowly and others fast—on purpose. Here’s why: 1. Fast transport is used for urgent or frequently needed materials: • Example: Neurotransmitters, vesicles, mitochondria • These are needed quickly at the synapse for communication. 2. Slow transport is used for long-lasting structural components: • Example: Cytoskeletal proteins (like tubulin and actin), enzymes • These don’t need to arrive quickly but are essential for maintaining the axon’s structure over time. Think of it like this: • Fast transport = express delivery (important things go first) • Slow transport = regular mail (stable parts that build or maintain the axon) So yes, neurons choose what goes fast and what goes slow—based on function and urgency.
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Resting membrane potential depends on what two thins and why is the cytoplasm more negative than the outside Note: to produce RMP of -70mV across the cell membrane, there is Relatively large net diffusion of K* outward and it establishes an equilibrium potential for K of -90 mV There is No diffusion of Anions across membrane Relatively small net diffusion of Na inward neutralizes some of the potential created by K+ alone
Usually the cytoplasm is negative(inside the cell) (-20 to - 110 mV; relative to the ECF = 0 mV) • Depends upon ions present: -Permeability -Electrochemical gradients The resting membrane potential (RMP) of most cells is between -20 mV to -110 mV, meaning the inside is more negative than the outside. • The extracellular fluid (ECF) is considered the reference point: 0 mV. • This negativity is due to: • More K⁺ inside, but it leaks out. • More Na⁺ and Cl⁻ outside, but Na⁺ entry is limited. • Large negatively charged proteins inside that cannot leave. • The Na⁺/K⁺ pump: pushes 3 Na⁺ out and 2 K⁺ in, making the inside more negative.
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Why is ionic ohms law (chord conductance equation) important? How is ionic ohms law different from goldman equation Look at a picture in the slide for the formula.
• Estimates membrane potential knowing equilibrium potentials and conductances for each ionic species in question: g= Conductance Conductance Depends only on the K channels being open or closed Equilibrium potential of the ion depends on the conc gradient of Kin and Kout This method focuses on conductance, which is dependent on whether channels (like potassium channels) are open or closed, and ion concentration gradients (for example, K⁺ inside vs. outside the cell Ionic ohms law= RMP or Vm is equal to the conductance of one ion x the equilibrium potential of that ion + the conductance of one ion x the equilibrium potential of another ion + the conductance of one ion x the equilibrium potential of a third ion if it’s there, etc ALL DIVIDED BY the conductances of all the ions present Conductance is a measure of how easily ions can flow across the membrane. • When ion channels are open, the conductance increases because ions can move through the membrane more easily. • The more open channels (e.g., K⁺ channels), the higher the conductance for that ion. 2. Equilibrium Potential (E_ion): • Each ion has its own equilibrium potential based on its concentration gradient across the membrane. NOTEEEEE: The equation takes a weighted average of the equilibrium potentials based on how permeable (conductive) the membrane is to each ion. • So, the greater the conductance for K⁺ (because more K⁺ channels are open), the closer the Vm will be to the E_K. Key Points: • The membrane potential (Vm) depends on the relative conductances of each ion. If K⁺ channels are open more than others, the membrane potential will be closer to E_K (around -90 mV). • If Na⁺ channels are open, the membrane potential will shift toward the E_Na (around +60 mV). Sure! Here’s a simpler breakdown of the two equations: Chord Conductance Equation (Ionic Ohm’s Law) • What it does: This equation calculates the resting membrane potential by looking at the conductance (how easy it is for ions to flow) and the equilibrium potential (the ideal voltage for each type of ion like K⁺, Na⁺, or Cl⁻). • How it works: It adds up the influence of each ion based on how open the channels are for that ion. The more channels for K⁺ that are open, the more the resting potential will be close to K⁺’s equilibrium potential. Goldman-Hodgkin-Katz (GHK) Equation • What it does: This equation is more detailed and calculates the resting membrane potential by considering both the concentration of ions inside and outside the cell and how easy it is for those ions to move across the membrane. • How it works: It takes into account not only how many channels are open but also the ion concentrations (like how much K⁺ is outside vs. inside) and permeability (how easily ions can cross the membrane). Key Differences in Simple Terms: • Chord Conductance: Looks mostly at how open the channels are for different ions (K⁺, Na⁺, Cl⁻) and uses their equilibrium potentials. • Goldman-Hodgkin-Katz: More complex. It looks at ion concentrations on both sides of the membrane, and how easy it is for each ion to pass through the membrane. In short, the GHK equation is a more precise and realistic way of calculating the membrane potential because it considers more factors (ion concentrations, permeability), while the Chord Conductance is a simpler estimate based mostly on conductance and equilibrium potentials. In Summary: • Permeability is about how well the membrane allows ion passage. • Conductance is about how easily the current can flow due to the ion’s movement across the membrane. Both terms are closely related but used in different contexts. Permeability is typically used in the Goldman-Hodgkin-Katz (GHK) equation, while conductance is used in the Chord Conductance equation to estimate membrane potential.
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Each ion will try to drive the potential towards its equilibrium potential • The ion with highest conductance wins over the one with lowest conductance. • The equation can simplified using only K+ and Na+ for the ionic ohms law equation why? Why is the RMP of a neuron close to -70mV using ionic ohms law to explain
The equation can be simplified using only K⁺ and Na⁺ because, at resting membrane potential, these two ions generally have the highest conductance compared to others like Cl⁻ or Ca²⁺. The permeability to K⁺ is typically much higher, meaning K⁺ has a stronger influence on the membrane potential. In simple terms: • K⁺ tends to dominate the resting membrane potential because it has the highest permeability under normal conditions. • Na⁺ contributes as well, but to a lesser extent compared to K⁺. • Other ions like Cl⁻ or Ca²⁺ usually have much lower conductance and thus play a smaller role in determining the resting potential. Got it! Here’s the same explanation written out in full sentences, without using the actual mathematical equation: At rest, a neuron’s membrane potential is mainly determined by potassium and sodium ions. Each of these ions has its own equilibrium potential — for potassium, it’s about minus 90 millivolts, and for sodium, it’s around plus 65 millivolts. Now, each ion tries to pull the membrane potential toward its own equilibrium potential. However, the strength of each ion’s influence depends on how easily it can move across the membrane, which we refer to as its conductance. At rest, the membrane is much more conductive to potassium than to sodium — in this example, the conductance ratio is seven to one in favor of potassium. This means potassium has a much stronger influence on the resting membrane potential than sodium does. So, when we calculate the resting membrane potential by taking into account the conductance and the equilibrium potentials of both ions, we find that the final value comes out to around minus 70.6 millivolts. This is why we usually say the resting potential is close to minus 70 millivolts — it’s because potassium, having the higher conductance, pulls the membrane potential closer to its own value. Let me know if you’d like this as a short summary too.
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If K+ channels suddenly open with no change in concentration gradient of other ions what happens to RMP? Na+ channels suddenly open with no change in concentration gradient of ther ions what happens to RMP? Why is potassium positively charged yet the inside is negative and sodium is positively charged and outside is positive Why is the equilibrium of potassium in a neuron at rest the same as the resting membrane potential of a neuron?
• If K+ channels suddenly open with no change in concentration gradient of other ions what happens to RMP? • It becomes more negative towards the K+ Equilibrium Potential and the cell is said to be hyperpolarized. Potassium channels are already leaky so if you open them suddenly, even more potassium will flow out so the cell will be more negative cuz more potosi let charged potassium is going out so there’s hyper polarization. It becomes lord close to the equilibrium potential of potassium so when the cell tried to pull K back inside cuz it’s too much outside, it makes the Ek closer to the equilibrium membrane potential of the resting potential of the cell You’ll see this is you use the ionic ohms law equation. Problem 2 Na+ channels suddenly open with no change in concentration gradient of ther ions what happens to RMP? becomes more positive towards the Na+ Equilibrium Potential and the cell is said to be depolarized. Note that at rest(no opening of channels) , sodium’s normal leaky channels has minimal effect because the membrane is barely permeable to Na⁺. Chat says: Potassium (K⁺) makes the cell interior more negative not because it’s more electronegative than sodium, but because it’s more permeable to the membrane so it leaks out easily, leaving behind trapped negative charges. Sodium (Na⁺) stays mostly outside due to low permeability, so it doesn’t balance the loss of positive charge. But in class, they said potassium is more electronegative than sodium that’s why. I’m a sense that it loses electrons more easily.
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Calculation 1 What happens to RMP in the cell of a patient who is severely hypokalemic? • Assume gK:gNa:gCl = 100:1:1 and [Na] = +65 mV and [Cl] = -70 mV. Note also that the K inside the cell is 150. The K in the hypokalemic patient is 3 and that of a normal person is 5
Even Without calculating, because the conductance or g of K is more than the other two ions, K will move out more that usually so the cell will be hyperpolarized. Cuz the cell doesn’t even get the chance to depolarize due the continuous and increased hyperpolarization So if you’re calculating, first calculate the Ek of K in a normal person and the hypokalemic person. Then find the RMP for the normal K and abnormal K So the Ek for the normal is -89 and the Abnormal is -102 The RMP of the normal K is -87 The RMP for the abnormal K is -100 You’re doing very well — let’s break it down and explain what it means clearly: First, definitions: • RMP (Resting Membrane Potential) is mainly set by K⁺, because the membrane is most permeable to K⁺ (gK = 100). • Ek (K⁺ equilibrium potential) gets more negative when outside K⁺ decreases, like in hypokalemia (from 5 → 3 mM). What you found: • Normal Ek ≈ –89 mV → RMP ≈ –87 mV • Hypokalemic Ek ≈ –102 mV → RMP ≈ –100 mV What this means: In severe hypokalemia, the RMP becomes more negative (hyperpolarized) — the cell is less excitable. Because: • Low K⁺ outside makes the gradient steeper → more K⁺ leaves the cell. • The inside becomes even more negative. • The cell is now further from threshold and harder to activate (less likely to fire an action potential). In short: Hypokalemia hyperpolarizes the RMP, making nerve and muscle cells less responsive, which can lead to muscle weakness, arrhythmias, or even paralysis If muscle cells have a hyperpolarized RMP, they cannot contract appropriately • This could lead to: •Paralysis (e.g. bicep, etc.) •Suffocation (e.g. diaphragm) •Asystole (e.g. heart) Want this summarized into a one-liner for memorization or an MCQ on it?
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What happens to RMP in the cell of a patient who is hyponatremic? • Assume gK:gNa:C/ = 100:1:1 and [K] = -90 mV and [CI] = -70 mV • Hint: calculate Ek values using normal and hypokalemic conc of K+ Na outside that is moving inside in the normal is 145 and the Na of the hyponatremic person is 150 and the one that’s already inside is 15.
The ENa (equilibrium of Na) is 59 The ENa of the abnormal sodium is 58 The RMp of the normal sodium is -88.34 The RMP of the abnormal sodium -88.35 So from this, we can see that the hyponatremia had negligible effect on the RMP of the cell. Cuz it’s Almost the same as though Na is normal in the body. The gradient for Nat decreases, causing ENa to become slightly more negative. • ENa changes are minimal. • RMP does not change appreciably. Why? Exactly — you’re on the right track! Here’s the explanation in simple terms: At rest, the neuron’s membrane is much more permeable to potassium (K⁺) than to any other ion, because it has many open potassium leak channels. This means K⁺ moves freely out of the cell, trying to reach its equilibrium potential (about –90 mV). Even though sodium (Na⁺) also has some leak channels, they are few, and the membrane isn’t very permeable to Na⁺ at rest. So its influence is small. Because K⁺ dominates, the resting membrane potential (~–70 mV) ends up being very close to potassium’s equilibrium potential, not sodium’s. In summary: Potassium controls the resting membrane potential because its leak channels are wide open and numerous, so the membrane potential stays near potassium’s equilibrium. Sodium’s influence is minor at rest. Great follow-up! In hyponatremia (low sodium in the extracellular fluid), you might expect it to strongly affect membrane potential — but here’s the key: At rest, Na⁺ has very little influence on the RMP, even in hyponatremia. Why? • The membrane at rest is barely permeable to Na⁺ (gNa is very low — usually around 1 compared to gK = 100). • So even if [Na⁺] outside drops, the RMP stays mostly controlled by K⁺. What changes can occur in hyponatremia? • The equilibrium potential for Na⁺ (ENa) becomes less positive. • This means that when Na⁺ channels open during depolarization, less Na⁺ enters, and action potentials may be smaller or slower to rise. • In severe cases, especially in the brain, this can cause swelling (due to water moving into cells), leading to confusion, seizures, or coma — but not due to changes in RMP, rather due to osmotic effects. In summary: Hyponatremia has little to no effect on RMP because Na⁺ permeability is low at rest. The danger in hyponatremia is osmotic swelling of cells, not major electrical changes in resting potential. Want a one-liner to memorize or an MCQ on this?
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What helps the cell more electrogenic? The pump can be inhibited by what two things? Why will you use one of the inhibitors to treat atrial fibrillation. What contributes more the the RMP?
The sodium potassium ATP pump. Revisiting the Na+-K+ ATPase (Na+-K* pump) Electrogenic (transfers positive charge out of cell) • 3 Nat out: 2 K+ in the pump Maintains gradients of Na+, K+  Note: Diffusion of ions down concentration gradients is the primary mechanism that maintains RMP!! Not the pump. The pump Utilizes ATP The pump can be Inhibitable by • cardiac glycoside; ouabain and digoxin If you inhibit it: Na⁺ builds up inside, and K⁺ decreases inside • Gradients collapse → membrane potential fades • Over time, the cell can’t generate action potentials or maintain its volume → can lead to cell dysfunction or death Long-term (like when the Na⁺/K⁺ pump is inhibited): • Na⁺ accumulates inside gradually. • K⁺ leaks out, but can’t be brought back in. • The ion gradients collapse — and without them: • No strong Na⁺ gradient = No strong depolarization • RMP fades • Neurons and muscle cells become less excitable, not more • Eventually, cells may die Analogy: Think of the Na⁺/K⁺ gradients like water pressure in a hose. If the pump breaks, pressure slowly drops — and even if you open the tap (Na⁺ channel), no water (Na⁺ current) flows well anymore. Excellent — and yes, the same inhibition of the Na⁺/K⁺ ATPase happens, but the context and dosage make the difference. Let’s break it down: In neurons (or generally): • If the Na⁺/K⁺ pump is completely blocked, Na⁺ builds up inside, K⁺ is lost, and over time the resting membrane potential collapses → cells lose excitability → cell death can occur. • This is why ouabain, a strong inhibitor of the pump, is toxic. In cardiac cells with digoxin: • Digoxin only partially inhibits the Na⁺/K⁺ pump. • It’s carefully dosed to allow: • Enough Na⁺ build-up to affect Ca²⁺ handling (improve contraction) • But not enough to completely collapse the gradients or cause toxicity. • This partial effect is therapeutic, not damaging (if within range). So the answer is: Yes — the same basic mechanism happens, but to a different degree — controlled with digoxin, toxic with full inhibition like with high-dose ouabain. Would you like a short analogy or visual to remember this difference better? The Na+-K*ATPase and Membrane Potential The role the of sodium-potassium pump on membrane potential is indirect. Pump itself makes only a small direct contribution (~20%) to membrane potential through its unequal transport of positive Most of the membrane potential (~80%) is cause by the diffusion of K+ and Nat down concentration gradients through
"background channels or leaky channels. Absolutely — here’s a simple breakdown to make this make sense: What the Na⁺-K⁺ pump (Na⁺/K⁺ ATPase) does: • Pumps 3 Na⁺ out of the cell • Brings 2 K⁺ in • Uses 1 ATP to do this • This movement is unequal (3 out, 2 in) → causes a net loss of +1 charge inside • This makes it electrogenic (helps make the inside a bit more negative) How it affects membrane potential: • This net movement of charge contributes a small part (~5–20 mV) of the resting membrane potential (RMP) • But the main contributor (80–95%) of the RMP is K⁺ diffusing out through leaky channels, not the pump directly Why the pump still matters a lot: • Even though it doesn’t make most of the RMP, it’s critical for maintaining the Na⁺ and K⁺ gradients • These gradients are what allow passive ion diffusion (like K⁺ leaving the cell) — and that’s what creates RMP • If the pump stops (e.g. with ouabain, a cardiac glycoside), gradients collapse → RMP fades → cell can’t function In short (to memorize): • The Na⁺-K⁺ pump maintains the ion gradients that allow RMP to exist. • It contributes a small direct part of the RMP by pumping 3 Na⁺ out and 2 K⁺ in (net + charge out). • But K⁺ leak is what mainly sets the RMP. Would you like an MCQ to reinforce this?
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1. Increased ECF K⁺ (Hyperkalemia) Which of the following changes is most likely to occur in a neuron during hyperkalemia? A. Hyperpolarization B. No change in RMP C. Depolarization D. Increased threshold potential 2. Increased ECF Na⁺ (Hypernatremia) What effect does an increase in extracellular sodium concentration have on the resting membrane potential? A. Hyperpolarization B. Depolarization C. No effect D. Membrane potential becomes positive 3. Decreased ECF K⁺ (Hypokalemia) What is the most likely effect of hypokalemia on the resting membrane potential of a muscle cell? A. Depolarization B. Hyperpolarization C. Action potential generation D. Increased sodium influx 4. Decreased ECF Na⁺ (Hyponatremia) Which of the following best describes the effect of hyponatremia on membrane potential? A. Depolarization B. Hyperpolarization C. No change D. Sodium moves into the cell 5. Increased ICF K⁺ What happens to the resting membrane potential when intracellular potassium concentration increases? A. Hyperpolarization B. Depolarization C. No effect D. Action potential initiation 6. Increased ICF Na⁺ How does an increase in intracellular sodium concentration affect the resting membrane potential? A. Hyperpolarization B. Depolarization C. No effect D. More potassium enters the cell 7. Decreased ICF K⁺ What is the expected effect on membrane potential if intracellular potassium levels fall? A. Depolarization B. Hyperpolarization C. No change D. Potassium influx increases 8. Decreased ICF Na⁺ What effect does decreased intracellular sodium have on the cell’s resting membrane potential? A. Depolarization B. Hyperpolarization C. No change D. Sodium influx decreases Let me know if you’d like the answers and explanations now.
Here are the correct answers and explanations for each MCQ: 1. Increased ECF K⁺ (Hyperkalemia) Correct Answer: C. Depolarization Explanation: High extracellular K⁺ reduces the concentration gradient between the inside and outside, so less K⁺ leaves the cell. This makes the inside less negative (i.e., depolarized). You thought: "More K⁺ outside means K⁺ won’t leave → buildup of negative charges inside → more negative = hyperpolarization." But in reality: The negative charge inside the cell is created by K⁺ leaving and leaving behind anions. So if K⁺ doesn't leave, then the cell stops getting as negative, and instead becomes more positive → depolarization. Situation What happens to K⁺ movement Effect on RMP Normal K⁺ leaves cell Inside becomes negative Hyperkalemia Less K⁺ leaves Inside becomes less negative → depolarization Hypokalemia More K⁺ leaves Inside becomes more negative → hyperpolarization 2. Increased ECF Na⁺ (Hypernatremia) Correct Answer: B. Depolarization Explanation: An increase in extracellular Na⁺ makes the driving force for Na⁺ influx stronger, which pushes the membrane potential toward Na⁺’s more positive equilibrium potential, leading to depolarization. 3. Decreased ECF K⁺ (Hypokalemia) Correct Answer: B. Hyperpolarization Explanation: When extracellular K⁺ is low, more K⁺ leaves the cell to balance the gradient, making the inside of the cell even more negative (hyperpolarized). 4. Decreased ECF Na⁺ (Hyponatremia) Correct Answer: B. Hyperpolarization Explanation: Lower extracellular Na⁺ reduces its inward driving force, slightly lowering its already small depolarizing effect at rest, so the cell becomes more negative (hyperpolarized). 5. Increased ICF K⁺ Correct Answer: A. Hyperpolarization Explanation: Higher intracellular K⁺ increases the concentration gradient, causing more K⁺ to leave the cell, making the inside more negative. 6. Increased ICF Na⁺ Correct Answer: A. Hyperpolarization Explanation: More Na⁺ inside the cell reduces the gradient for Na⁺ influx, lessening its depolarizing influence, so the cell becomes slightly more negative. 7. Decreased ICF K⁺ Correct Answer: A. Depolarization Explanation: Lower intracellular K⁺ reduces the gradient, so less K⁺ exits the cell, leading to less negative charge inside — depolarization. 8. Decreased ICF Na⁺ Correct Answer: A. Depolarization Explanation: Less intracellular Na⁺ increases the gradient for Na⁺ to enter the cell, enhancing its depolarizing effect. Let me know if you’d like to turn these into flashcards or quiz yourself on them. Changes in Membrane Potential due to Pathophysiological Changes in Total lon Concentrations in the ECF or ICF • Increased ECF K* (Hyperkalemia) = depolarization • Increased ECF Na* (Hypernatremia) = depolarization • Decreased ECF K* (Hypokalemia) = hyperpolarization • Decreased ECF Na* (Hyponatremia) = hyperpolarization • Increased ICF K+ = hyperpolarization • Increased ICF Na+ = hyperpolarization • Decreased ICF K+ = depolarization • Decreased ICF Na+ = depolarization
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What is a membrane potential of a cell? Note that the magnitude of this potential still depends on the degree of separation of the opposite charges. State two types of potentials State the three ions responsible for generation RMP Note: K moving from outside to the ICf is active and K moving from the ICF to the outside is passive Na moving from the outside to the ICF is passive and moving it from ICF to ECF is active transport
ELECTRICAL ACTIVITY OF THE CELL • Membrane potential: the membrane potential of a cell reflects the separation of charges across the cell membrane (unequal distribution). In simple terms: The membrane potential is like a tiny battery. It happens because there are more positive or negative charges on one side of the cell membrane than the other. This difference in charge is what creates the membrane potential. • Measured in millivolts (mV). • The magnitude of the potential depends on the degree of separation of the opposite charges. • Types of potentials • Resting membrane potential (RMP): = about - 70m V • Action potential (AP) • The ions responsible for generating RMP are Nat, K+ and A-(intracellular proteins)
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What is the Gibbs Donovan effect What is chemical gradient and electrical gradient How are they and needn’t equation related to Gibbs Donovan effect
The Gibbs-Donnan equation describes the equilibrium distribution of ions across a semipermeable membrane when one side contains non-diffusible, charged molecules (like proteins) and the other side does not Or it talks about what happens when one side has charged molecules that can’t move and the other side has charged molecules that can move Great question — and let’s clear that up! Actually, proteins are not permeable across the membrane. That’s the key! What I meant was: The presence of impermeable (trapped) proteins inside the cell causes permeable ions like Na⁺, K⁺, and Cl⁻ to redistribute unevenly across the membrane. Example: • Proteins (negatively charged) are stuck inside the cell. • To balance this negative charge, more K⁺ (a positive ion) stays inside the cell. • Cl⁻, a negative ion, might be repelled from the inside and stay outside more. • This results in unequal (uneven) distribution of permeable ions like K⁺ and Cl⁻ across the membrane. That’s the Donnan effect — all caused by trapped proteins influencing how other ions are distributed. Would you like a one-line summary to memorize? In summary: • Donnan equilibrium explains how trapped proteins inside the cell cause uneven ion distribution (ionic gradients). • This ionic gradient creates both: • A chemical force (Fc): ions want to move from high to low concentration. • An electrical force (Fe): ions feel pushed or pulled by charge differences. • The Nernst equation calculates the membrane potential where these two forces are balanced for a single ion. • So: Donnan explains the origin of gradients, Fc and Fe are the two forces that arise from the gradients, Nernst tells us the voltage needed to keep the ion still. Let me know if you want a short MCQ based on this. Here’s a very simple version: • Donnan equilibrium happens because some big proteins inside the cell can’t move out. • These trapped proteins attract some ions and push others away. • This creates uneven amounts of ions inside and outside the cell — that’s the ionic gradient. • Because ions have charges, this also creates an electric difference across the membrane. • The Nernst equation tells us what that electric difference (voltage) would be for one ion if it was balanced. So: Proteins trapped → ions shift → charge builds up → voltage happens. Would you like a quick example to make it clearer? the Nernst equation calculates the electrochemical equilibrium potential for ions. It’s just that it does it for one ion at a time, which is why we use it to figure out where each ion would “want” to be, voltage-wise. To recap: • Electrochemical difference is what drives ions to move. • The Nernst equation calculates the exact equilibrium point for one ion, where the concentration and electrical forces are balanced Absolutely! Let’s break this down simply: What’s happening at the membrane? There are different concentrations of ions (like K⁺) on each side of the membrane, which creates two forces: 1. Chemical Gradient (Fc) • Ions want to move from where there’s more of them to where there’s less (high to low concentration). • This is like diffusion. • For example, if there’s more K⁺ outside than inside, K⁺ wants to move into the cell. • This force is calculated with: Fc = RT ln([K⁺ outside] / [K⁺ inside]) 2. Electrical Gradient (Fe) • Positive and negative charges attract. • If the inside of the cell is negative, positive ions like K⁺ will be pulled in by the electrical force. • This force is: Fe = zFE where z = charge on the ion (e.g., +1 for K⁺), F = Faraday’s constant, E = membrane potential When do these forces balance? • When chemical and electrical forces are equal and opposite, the ion stops moving. • This balance point is the equilibrium potential (E) — what the Nernst equation calculates. Nernst Equation (Simple Purpose): It tells us the membrane voltage (E) needed to balance an ion’s concentration difference so it stays still (no net movement). Gibbs-Donnan Equilibrium: This happens when large charged molecules (like proteins) can’t cross the membrane but still affect ion distribution. • The ions rearrange on both sides to maintain electrical neutrality, causing uneven ion distribution. • It helps explain why cells have more K⁺ inside and more Na⁺ outside even though only some ions can move freely. Would you like a visual or diagram to make this even clearer? Great — let’s make the Gibbs-Donnan equilibrium super simple: Imagine This: • You have a cell membrane with two sides: inside and outside. • The membrane is semi-permeable: Small ions (like Na⁺, K⁺, Cl⁻) can move across it. But large molecules, like proteins (usually negatively charged), can’t move across. Here’s the Key Problem: • Inside the cell: you have trapped negatively charged proteins (like albumin). • These proteins pull in positive ions like K⁺ to balance their negative charge. • But now there are more particles inside, which causes water to enter and could make the cell swell. What the Cell Does: • To avoid swelling and electrical imbalance, the other ions (like Cl⁻, Na⁺) redistribute. • This uneven distribution of ions across the membrane, caused by the trapped protein, is what we call Gibbs-Donnan equilibrium. In short: Gibbs-Donnan equilibrium explains how uncharged but trapped molecules (like proteins) cause an uneven distribution of permeable ions across a membrane to maintain electrical and osmotic balance. Let me know if you want a simple analogy or drawing to help solidify it!
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State and explain fhe characteristics of action potentials What shape is the action potential in nerve cells and the shape in cardiac cells What causes these shapes?
Excitable tissues: Capable of producing electrical signals when stimulated and undergo transient, rapid changes in their membrane potential. • Nerve cell (receive, process and transmit messages) • Muscle cell ( contraction). Characteristics of action potential • Stereotypical size and shape • Propagation • All or none response Shape in nerve cells is spike shaped (the man said bell shaped sha) and in cardiac cells it’s sort of bell shaped with a plateau. a quick, sharp rise and fall (a “spike”) in nerve cells while in cardiac cells, it includes a prolonged plateau phase (Phase 2) for depolarization resulting in a more gradual “bell-shaped” curve The bell or plateau thing is due to voltage gated K channels opening slowly affecting the rate of repolarization and then the presence of voltage gated sodium calcium channels. The impact of sodium calcium channels or L type calcium channels in the cardiac cells is much slower than that of sodium channels in the cardiac cells that’s why they and the slow opening potassium channels are responsible for or maintain the plateau. Yes, you’re absolutely right! Let’s break it down in simple terms. In cardiac cells, the action potential has a characteristic plateau phase, and it’s shaped by two main factors: 1. Slow opening of voltage-gated potassium (K⁺) channels: • When the cell depolarizes, potassium channels slowly open, allowing K⁺ to leave the cell. However, this happens gradually, which slows down repolarization (the process of the cell returning to its resting state). This results in the plateau phase that you see in the action potential. 2. Sodium-Calcium (Na⁺-Ca²⁺) channels: • In addition to potassium channels, there are voltage-gated sodium-calcium (Na⁺-Ca²⁺) channels that open during the action potential, allowing calcium ions (Ca²⁺) to enter the cell. However, these channels open more slowly than the voltage-gated sodium (Na⁺) channels in nerve cells. • The slower calcium influx helps maintain the depolarization (the plateau), as calcium counters the potassium ions trying to exit the cell. This creates a prolonged depolarization phase, preventing early repolarization and ensuring a sustained contraction in the heart muscle. In summary: • The bell-shaped curve of the action potential in nerve cells is due to the rapid rise and fall of sodium and potassium movements. • The plateau phase in cardiac cells is due to the slow opening of potassium channels (which delays repolarization) and the influx of calcium ions through sodium-calcium channels, which helps maintain depolarization for a longer period. The sodium-calcium channels in cardiac cells are indeed slower than the regular sodium channels found in nerve cells, but their presence and the slow calcium entry are crucial for the plateau phase, which is essential for proper heart function. Nerve cell action potential: No, the action potential in nerve cells is not bell-shaped. It follows a characteristic spike-like shape with distinct phases. Here’s a simplified breakdown: 1. Resting Phase: The neuron is at rest, and the membrane potential is around -70 mV. 2. Depolarization or rising phase : When a stimulus triggers the opening of sodium (Na⁺) channels, sodium ions rush into the cell, making the inside more positive. This causes the membrane potential to become more positive, reaching around +30 mV. This is the rising phase. 3. Repolarization or falling phase : Potassium (K⁺) channels open, and potassium ions exit the cell, causing the membrane potential to return to negative (more like the resting state). 4. Hyperpolarization: Sometimes, the membrane potential becomes even more negative than the resting potential due to continued potassium efflux. This is the falling phase. 5. Return to Resting Potential: Eventually, the membrane potential returns to its resting state, ready for the next action potential. So, the shape of an action potential is more like a sharp spike, with rapid depolarization followed by repolarization, rather than a bell shape. Cardiac cell action potential: In cardiac cells, the action potential has a different shape compared to nerve cells. It is typically described as having five distinct phases that give it a plateau or a prolonged depolarization phase, which is more like a “bell-shaped” or “spike with a plateau” curve. Here’s a breakdown: 1. Phase 0 (Depolarization): Similar to nerve cells, sodium (Na⁺) channels open, and sodium rushes into the cell, causing a rapid depolarization. The membrane potential becomes more positive, reaching up to +30 mV. 2. Phase 1 (Initial Repolarization): Sodium channels close, and potassium (K⁺) channels open, causing a brief outflow of K⁺. This causes the membrane potential to briefly dip before plateauing. 3. Phase 2 (Plateau Phase): This is the characteristic phase of the cardiac action potential. Sodium Calcium (Ca²⁺) channels open, allowing calcium to flow into the cell, while potassium continues to exit. The influx of calcium balances the efflux of potassium, causing a plateau in the membrane potential. This phase is crucial for the contraction of the heart muscle (systole). 4. Phase 3 (Repolarization): Calcium channels close, and potassium channels remain open. Potassium ions flow out of the cell, causing the membrane potential to return to a more negative state. 5. Phase 4 (Resting Potential): The cell is at rest, and the membrane potential is restored to the baseline, typically around -90 mV, until the next action potential. The plateau phase (Phase 2) is what differentiates cardiac action potentials from nerve action potentials and gives them a more “bell-shaped” appearance. This extended depolarization helps in the coordination of heart muscle contraction and prevents the heart from undergoing rapid, unnecessary contractions (i.e., it helps prevent arrhythmias).
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State and explain the factors that affect the movement of action potentials along the axon to the axon terminal
The axon isn’t a hollow tube but it’s a tube. 1. Cytoplasmic resistance 2.membrane of axon resistance 3.length of axon 4. Membrane capacitance(the capacitance means more charges to depolarize the membrane. Capacitors store and separate charges) Here’s a simple breakdown of how each of those factors affects the speed (velocity) of an action potential traveling along a nerve fiber: 1. Cytoplasmic Resistance (Internal Resistance) • This is the resistance to the flow of electrical current inside the axon. • Lower resistance = easier for current to flow = faster conduction. • If the inside of the axon is very “crowded” or narrow (like a thin straw), it slows things down. So: lower cytoplasmic resistance = faster action potential. That’s a very logical thought, and you’re right to consider how resistance might work — but here’s the key distinction: In nerves, conduction speed is not limited by cytoplasmic resistance alone, but rather by a combination of: 1. Internal (axoplasmic) resistance – Yes, thicker fibers have more cytoplasm, but the resistance actually decreases with increased diameter. Why? Because resistance is inversely proportional to the cross-sectional area. A thicker fiber has a larger area, so axoplasmic resistance decreases. Think of it like water through a pipe: a wide pipe (thick fiber) lets more water through easily — same for current in nerves. 2. Membrane resistance and capacitance – Thicker fibers often have more myelin, which acts as an insulator. Myelination and fiber diameter together increase conduction speed. Summary: • Thicker nerve fibers = lower internal resistance + often myelinated = faster conduction • Thinner nerve fibers = higher resistance + often unmyelinated = slower conduction So the correct understanding is: thicker = faster, not slower. You’re thinking like a scientist — just needed this one tweak in concept. Want a simple diagram to visualize this? 2. Membrane Resistance (Resistance across the axon membrane) • This determines how easily current can leak out of the axon. • Higher membrane resistance means less leakage, so the signal stays strong and travels farther before needing a boost. So: higher membrane resistance = faster conduction. 3. Length of the Axon • Longer axons can slow down conduction if they’re not well-insulated (like with myelin). • But if the axon is myelinated, this effect is reduced because the signal jumps (saltatory conduction) between nodes. So: longer axon = slower conduction, unless well-insulated. 4. Membrane Capacitance • Capacitance is how much charge the membrane can store. • High capacitance means more charge is needed to change the membrane potential, which slows depolarization. • Myelin reduces membrane capacitance, helping speed up conduction. So: lower membrane capacitance = faster conduction. In Summary: Factor Effect on Speed Low cytoplasmic resistance Faster conduction High membrane resistance Faster conduction Shorter axon length Faster conduction Low membrane capacitance Faster conduction Would you like a diagram to visualize this?
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Explain saltatory conduction State five examples of demyelination diseases
Myelin increases membrane resistance and this increases the velocity of action potentials cuz they’re not likely to leak. This means you’ll process info faster and have faster reflexes. Demyelination diseases reduce velocity Yes — demyelinating diseases, like multiple sclerosis, reduce the velocity of action potentials. Here’s how that ties into saltatory conduction: Saltatory Conduction (in simple terms): • In myelinated axons, the myelin sheath (made by Schwann cells or oligodendrocytes) insulates the axon. • This prevents charge from leaking out and reduces membrane capacitance. • Action potentials don’t happen continuously along the whole axon. Instead, they “jump” from one Node of Ranvier to the next — these are small gaps between myelinated segments. • These nodes are rich in voltage-gated Na⁺ channels, so depolarization happens only there, making conduction much faster and more energy-efficient. What happens in demyelination: • Myelin is damaged or lost, so: • Leakage of ions increases (lower membrane resistance). • Capacitance increases — more charge is needed to depolarize the membrane. • The “jumping” stops, and conduction becomes slower or even blocked. • The axon may fail to reach threshold, leading to signal failure. In short: • With myelin: signal jumps — fast, efficient. • Without myelin: signal crawls — slow, or blocked. Would you like a simple comparison chart or drawing of this process? Here are some common demyelinating diseases: Central Nervous System (CNS) Demyelinating Diseases: 1. Multiple Sclerosis (MS) – most common; immune system attacks myelin in the brain and spinal cord. 2. Neuromyelitis Optica (Devic’s disease) – affects optic nerves and spinal cord. 3. Acute Disseminated Encephalomyelitis (ADEM) – often post-infection or post-vaccine; rapid onset. 4. Progressive Multifocal Leukoencephalopathy (PML) – caused by JC virus, often in immunocompromised individuals. 5. Central Pontine Myelinolysis – often due to rapid correction of low sodium levels. Peripheral Nervous System (PNS) Demyelinating Diseases: 1. Guillain-Barré Syndrome (GBS) – autoimmune, rapid-onset muscle weakness; attacks peripheral myelin. 2. Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) – chronic form of GBS. 3. Charcot-Marie-Tooth Disease (some types) – genetic, affects peripheral nerves. Would you like a way to easily remember these?
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Note: lonic basis of action potential • Rest or polarisation (charges are separated) • Depolarisation (less -ve, more +ve) • Repolarisation (returning to rest) • Hyperpolarisation (more -ve than RMP) State the two main Refractory periods What are the two main types of synaptic transmission? How does an electrical synapse transmit signals? What structure is involved in chemical synaptic transmission? What type of synaptic arrangement is found at the neuromuscular junction? What is an EPSP? Excitatory Postsynaptic Potential What is an IPSP?Inhibitory Postsynaptic Potential What is spatial summation? What is temporal summation?
• Absolute refractory period: Na channels inactive • Relative refractory period: Higher K+ conductance than at rest Yes, that’s correct! Here’s a simplified explanation: Absolute Refractory Period • Why?: Sodium (Na⁺) channels are inactivated, not just closed. • Result: No matter how strong a stimulus is, no new action potential can be started. Relative Refractory Period • Why?: Some Na⁺ channels have recovered, but potassium (K⁺) channels are still open, making the membrane more negative than usual (hyperpolarized). • Result: A stronger-than-normal stimulus is needed to trigger an action potential. Would you like a visual diagram or a mnemonic for these? Q1: What are the two main types of synaptic transmission? A1: Electrical synapse and chemical synapse. Q2: How does an electrical synapse transmit signals? A2: Through gap junctions that allow direct flow of ions between cells. Q3: What structure is involved in chemical synaptic transmission? A3: The synaptic cleft, where neurotransmitters are released. Q4: What type of synaptic arrangement is found at the neuromuscular junction? A4: One-to-one synaptic arrangement. Q5: What is an EPSP? A5: Excitatory Postsynaptic Potential—brings the membrane potential closer to threshold. Q6: What is an IPSP? A6: Inhibitory Postsynaptic Potential—moves the membrane potential away from threshold. Q7: What is spatial summation? A7: When multiple inputs fire at the same time to influence the postsynaptic neuron. Q8: What is temporal summation? A8: When one input fires repeatedly over time to influence the postsynaptic neuron. Here’s a simple summary of the key points you listed about propagation and synaptic transmission: Propagation of Action Potential • Action potentials travel along a nerve or muscle fiber through local currents. Types of Synaptic Transmission 1. Electrical Synapse • Uses gap junctions • Very fast and direct (no neurotransmitters) • Common in some brain regions and heart muscle 2. Chemical Synapse • Uses a synaptic cleft and neurotransmitters • Slower but more controlled • Most common type in the nervous system Synaptic Arrangements • One-to-One: One neuron to one target (e.g., neuromuscular junction) • One-to-Many: One neuron affects multiple targets • Many-to-One: Many neurons affect one target Postsynaptic Potentials • Excitatory Synapse • Makes the postsynaptic membrane closer to threshold • Generates an EPSP (Excitatory Postsynaptic Potential) • Inhibitory Synapse • Makes the membrane more negative (further from threshold) • Generates an IPSP (Inhibitory Postsynaptic Potential) Summation • Temporal Summation: One input firing repeatedly over time • Spatial Summation: Multiple inputs firing at the same time Yes — your notes are exactly right! Here’s a simple clarification: Spatial Summation(this type is usually used to generate an action potential and depolarization out of a weak stimuli) • Definition: Multiple stimuli from different neurons (or locations) arrive at the same time at different synapses on the same postsynaptic neuron. • Think of it as: “Many friends knocking on different doors of the same house at once.” • Result: Their combined effect brings the neuron to threshold (or closer). Temporal Summation • Definition: One neuron fires repeatedly over time at the same synapse, allowing effects to build up. • Think of it as: “One friend knocking quickly and repeatedly on the same door.” • Result: If the knocks come fast enough, they can trigger an action potential. Would you like flashcard-style questions for these too?
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Sure! Here are just the flashcard questions: 1. What is a tripartite synapse? 2. What is a 4-part (quadpartite) synapse? 3. Where are most neurotransmitter vesicles stored — in the terminal or the spine? 4. Why are glial cells close to synapses in the hippocampus? 5. What is priming in synaptic transmission? 6. What is docking in synaptic transmission? 7. What is an excitatory postsynaptic potential (EPSP)? 8. What do autoreceptors on presynaptic neurons do? 9. What is the glutamate-glutamine shuttle?
Here’s a flashcard-style set for everything you just asked about: Flashcard 1 Q: What is a tripartite synapse? A: A synapse involving the presynaptic neuron, postsynaptic neuron, and an astrocyte. Flashcard 2 Q: What is a 4-part (quadpartite) synapse? A: A synapse involving the presynaptic neuron, postsynaptic neuron, an astrocyte, and a microglial cell. Flashcard 3 Q: Where are most neurotransmitter vesicles stored — in the terminal or the spine? A: In the presynaptic terminal. Flashcard 4 Q: Why are glial cells close to synapses in the hippocampus? A: To help clear neurotransmitters, regulate the environment, and support neuronal function. Flashcard 5 Q: What is priming in synaptic transmission? A: The process of preparing vesicles in the presynaptic terminal for release. Flashcard 6 Q: What is docking in synaptic transmission? A: When a primed vesicle attaches to the presynaptic membrane, ready to release its contents. Flashcard 7 Q: What is an excitatory postsynaptic potential (EPSP)? A: A small depolarization in the postsynaptic neuron that brings it closer to threshold. Flashcard 8 Q: What do autoreceptors on presynaptic neurons do? A: They detect released neurotransmitters and reduce further release when levels are high. Flashcard 9 Q: What is the glutamate-glutamine shuttle? A: Glutamate is taken up by astrocytes, converted to glutamine, returned to the neuron, and converted back to glutamate. Would you like a downloadable version of these flashcards (e.g., for Anki or Quizlet)? Great points — you’re touching on advanced neuroscience concepts! Let’s break everything down in very simple terms: 1. Tripartite Synapse • A tripartite synapse includes: • The presynaptic neuron • The postsynaptic neuron • A nearby astrocyte (a type of glial cell) • Astrocytes help regulate neurotransmitter levels (like glutamate), support the neurons, and influence the strength of the signal. 2. 4-Part Synapse • Also called the “quadpartite synapse”. • Adds microglia to the tripartite synapse. • So it includes: • Presynaptic neuron • Postsynaptic neuron • Astrocyte • Microglia (involved in immune response and pruning synapses) 3. More Vesicles in Terminal Than in Spine • Presynaptic terminals store lots of neurotransmitter-filled vesicles ready for release. • Spines on the postsynaptic side (like dendritic spines) mainly receive signals — they don’t store vesicles. 4. Glial Cells Near Synapses in Hippocampus • In the hippocampus, astrocytes are very close to synapses. • They control glutamate levels, take up extra neurotransmitters, and help keep the environment stable. 5. Priming and Docking • Priming: Prepares vesicles in the presynaptic terminal to be ready for release. • Docking: The vesicle attaches to the membrane, ready to release neurotransmitters into the synaptic cleft. (Note: Docking happens in the presynaptic terminal, not postsynaptic. You may have mixed up that part.) 6. Excitatory Postsynaptic Potential (EPSP) • When excitatory neurotransmitters (like glutamate) bind to receptors on the postsynaptic neuron, it becomes less negative (closer to threshold). • This small change is called an EPSP — it encourages firing. 7. Autoreceptors • Autoreceptors sit on the presynaptic neuron. • They detect how much neurotransmitter (like glutamate or dopamine) has been released. • If too much is out, they slow down further release — like a feedback brake. 8. Glutamate-Glutamine Shuttle • Glutamate (excitatory neurotransmitter) is taken up by astrocytes after it’s released. • Astrocytes convert it to glutamine (non-toxic). • Glutamine goes back to the presynaptic neuron and is converted back to glutamate — ready to use again.
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Sure! Here are just the flashcard questions: 1. What is the Gate Control Theory of pain? 2. Which fibers are responsible for inhibiting pain signals in the Gate Control Theory? 3. What type of neurons are involved in inhibiting pain transmission in the spinal cord? 4. What is lateral inhibition in the context of pain modulation? 5. How does rubbing a painful area reduce pain sensation?
Here are flashcard-style questions based on the topic: Q1: What is the Gate Control Theory of pain? A1: It’s the idea that non-painful input can inhibit the transmission of pain signals to the brain by “closing the gate” in the spinal cord. Q2: Which fibers are responsible for inhibiting pain signals in the Gate Control Theory? A2: A-beta fibers, which carry non-painful touch signals. Q3: What type of neurons are involved in inhibiting pain transmission in the spinal cord? A3: Inhibitory interneurons. Q4: What is lateral inhibition in the context of pain modulation? A4: It’s when inhibitory neurons suppress the activity of neighboring neurons to reduce the spread or intensity of a signal, such as pain. Q5: How does rubbing a painful area reduce pain sensation? A5: It activates A-beta fibers, which stimulate inhibitory interneurons that suppress pain signals. Here’s a brief explanation: Inhibitory Signals in Pain Modulation: • Gate Control Theory (Melzack and Wall): This theory proposes that non-painful stimuli (like touch or pressure) can inhibit pain signals in the spinal cord before they reach the brain. • Lateral Inhibition: Nearby inhibitory interneurons reduce the transmission of pain by inhibiting secondary pain neurons. For example, rubbing a bumped elbow activates A-beta fibers, which trigger inhibitory interneurons that “close the gate” to pain signals coming from slower C fibers. • Result: The brain perceives less pain due to this inhibition at the spinal cord level. Would you like a diagram or flashcard question for this?