unit 2 week 2 pt 1 Flashcards
What is irritability in organisms?
Irritability is the property where all organisms respond to external stimulation.
What are nerve cells also known as?
Nerve cells are also known as neurons.
What are the basic parts of a neuron?
The basic parts of a neuron are the cell body, dendrites, axon, terminal knob (aka axon terminals), and myelin sheath. Node of ranvier speeds up signal, myelin insulates/protects
What is the function of the cell body in a neuron?
The cell body is where the nucleus is located, acts as the metabolic center, and is the site where material contents are made.
What do dendrites do?
Dendrites receive incoming information from external sources, typically other neurons.
What is the role of the axon?
The axon conducts outgoing impulses away from the cell body and toward the target cell(s).
What is the terminal knob?
The terminal knob is a specialized site where impulses are transmitted from a neuron to the target cell.
What is the myelin sheath?
The myelin sheath is the lipid-rich material wrapped around most neurons in the vertebrate body. originates from schwann cells
What is voltage?
Voltage is the electric potential difference.
What is membrane potential?
Membrane potential is the electrical potential difference across a membrane, which exists in all cells.
What is resting potential?
Resting potential is the electrical potential difference measured for an excitable cell when it is not subject to external stimulation.
What is the typical resting potential of a nerve cell?
The resting potential is typically around -70 mV (inside negative relative to outside).
How is resting potential measured?
Resting potential is measured by inserting a microelectrode into the cytoplasm and another in the extracellular fluid, then using a voltmeter to record the potential difference.
How is resting potential established?
The Na+/K+ ATPase pump moves 3 Na+ out and 2 K+ in, creating ion concentration gradients. Most ion channels are closed, but K+ leak channels allow K+ to diffuse out, making the inside more negative.
What equation determines the equilibrium potential of an ion?
The Nernst equation calculates the equilibrium potential for an ion (E_ion) based on its concentration difference.
Notes:
-R = gas constant
-T = temperature
-z= charge of the ion
-F = Faraday’s constant
-[K+]o[K^+]_o[K+]o and [K+]i[K^+]_i[K+]i = extracellular and intracellular K+ concentrations
Why is the resting potential close to the K+ equilibrium potential?
Since K+ is the most permeable ion, its movement dominates. The calculated K+ equilibrium potential is around -91 mV, while the actual resting potential is -70 mV, slightly less negative due to Na+ leak channels.
What is the Na+ equilibrium potential?
The Na+ equilibrium potential, calculated using the Nernst equation, is +55 mV, much higher than the resting potential.
Why does K+ stop diffusing out at equilibrium?
At equilibrium, two opposing forces balance each other: the concentration gradient drives K+ out, while the electrical gradient pulls K+ back in.
-At equilibrium, no net movement of K+ occurs.
What is depolarization?
Depolarization is a decrease in the electrical potential difference across a membrane. The process where the inside of a cell becomes less negatively charged compared to the outside, effectively reducing the difference in electrical charge across the cell membrane.
What is the threshold in action potentials?
The threshold is the point during depolarization of an excitable cell where voltage-gated sodium channels open, resulting in Na+ influx and a brief reversal in membrane potential.
What is an action potential?
-a brief reversal of the electrical charge across a cell membrane, from a negative resting state to a positive state, followed by a return to the resting state.
-How it works:
Depolarization: It begins with a stimulus that causes a sudden influx of positively charged sodium ions (Na+) into the cell, making the cell’s interior more positive than the outside.
Repolarization: The influx of sodium ions is followed by an efflux of positively charged potassium ions (K+), which restores the negative charge inside the cell.
Hyperpolarization: The membrane potential can briefly overshoot the resting state (hyperpolarization) before returning to the baseline.
All-or-none principle:
Action potentials follow an “all-or-none” principle, meaning they either occur fully, or not at all, unlike graded potentials which vary in strength.
What research led to our understanding of action potentials?
Hodgkin, Huxley, and Katz studied the giant squid axon in the 1940s-50s, which was large enough to measure electrical activity effectively.
What triggers an action potential?
A stimulus opens some sodium (Na+) channels, allowing Na+ to enter the neuron. If the membrane reaches the threshold (~-50 mV), more Na+ channels open, triggering the action potential.
-basically: reaching the threshold
What are the phases of an action potential?
The phases are: 1) Depolarization: Na+ enters, making the inside more positive (~+40 mV). 2) Repolarization: Na+ channels close, K+ channels open, allowing K+ to exit. 3) Hyperpolarization: The membrane briefly becomes more negative than its resting state.
What is the role of the Na+/K+ ATPase pump?
The Na+/K+ ATPase pump restores the original balance of Na+ and K+ after multiple action potentials.
Why is the action potential an ‘all-or-none’ event?
If the threshold is reached, an action potential always occurs. If not, nothing happens—there’s no partial response.
What is the refractory period?
The refractory period is the time after firing when a neuron cannot fire again immediately, ensuring proper timing of nerve signals.
How do local anesthetics block nerve signals?
Local anesthetics like procaine and novocaine block Na+ channels, preventing neurons from firing and stopping pain signals.
What is a nerve impulse?
An action potential, also called a nerve impulse, is an electrical charge that travels along the membrane of a neuron.
How does an action potential travel?
Once triggered, an action potential propagates down the neuron as a nerve impulse to reach the nerve terminals.
Why does an action potential continue along the neuron?
The large depolarization at one site creates a charge difference across the membrane, causing local ion movement that depolarizes the next region and triggers a new action potential.
AKA, in other words…
An action potential continues along a neuron because the depolarization caused by the influx of sodium ions triggers the opening of voltage-gated sodium channels in adjacent regions of the axon membrane, creating a wave-like propagation of electrical signals.
How do we detect differences in stimulus strength?
A stronger stimulus activates more neurons, triggers high-threshold neurons, and increases action potential frequency.
How does axon diameter affect conduction speed?
Larger axons allow for faster conduction due to lower resistance to ion flow.
How does myelination improve conduction?
Myelination prevents ion leakage, forcing action potentials to occur only at nodes of Ranvier, allowing impulses to jump and reach speeds of 120 m/s—20x faster than in unmyelinated neurons.
What happens when myelin is damaged?
In multiple sclerosis (MS), myelin deteriorates, slowing or stopping nerve impulses, leading to symptoms like muscle weakness and vision problems.
What are synapses?
Synapses are specialized junctions of a neuron with its target cell.
What is the synaptic cleft?
The synaptic cleft is the gap between the presynaptic neuron (the neuron sending the signal) and the postsynaptic neuron (the neuron receiving the signal).
IN OTHER WORDS…
The synaptic cleft, also known as the synaptic gap, is the small space between the axon terminal of one neuron and the dendrite (or other part of the receiving neuron) where neurotransmitters are released to transmit signals.
What is a presynaptic cell?
A presynaptic cell is a receptor cell or a neuron that conducts impulses toward a synapse.
What is a postsynaptic cell?
A postsynaptic cell is a neuron, muscle, or gland cell that receives signals on the other side of the synapse.
What are neuromuscular junctions?
Neuromuscular junctions are points of contact between the terminus of an axon and a muscle fiber, where nerve impulses are transmitted.
What are synaptic vesicles?
Synaptic vesicles serve as storage sites for the chemical transmitters that act on postsynaptic cells
AKA…
-small, membrane-bound organelles found in the presynaptic terminal of neurons. They play a crucial role in the transmission of nerve impulses by storing and releasing neurotransmitters.
What are neurotransmitters?
Neurotransmitters are chemicals released from a presynaptic terminal that bind to the postsynaptic target cell, altering its membrane potential.
What’s a synapse?
a specialized junction where a presynaptic neuron communicates with a postsynaptic cell
How do neurons communicate across a synapse?
Neurons communicate across a synapse via chemical neurotransmitters, which diffuse across the synaptic cleft.
What are presynaptic and postsynaptic cells?
-The presynaptic cell (a neuron or receptor cell) sends impulses toward the synapse.
-The postsynaptic cell (a neuron, muscle, or gland cell) receives the signal.
What are neuromuscular junctions?
These are synapses between motor neurons and skeletal muscle cells, where neurotransmitters stimulate muscle contraction.
How does an impulse trigger neurotransmitter release?
- An action potential reaches the terminal knob of the presynaptic neuron.
- Voltage-gated Ca²⁺ channels open, allowing Ca²⁺ ions to enter.
- Increased Ca²⁺ concentration causes synaptic vesicles to fuse with the membrane.
- Neurotransmitters are released into the synaptic cleft.
What happens after neurotransmitters are released?
Neurotransmitters bind to receptors on the postsynaptic cell, leading to either excitation or inhibition. [details: excitation refers to processes that increase the likelihood of a neuron firing, while inhibition refers to processes that decrease the likelihood of a neuron firing]
How do neurotransmitters excite or inhibit the postsynaptic cell?
Excitatory neurotransmitters open cation channels, allowing Na+ to enter, while inhibitory neurotransmitters open anion channels, allowing Cl- to enter. [details: Excitatory signals increase the membrane potential of a neuron, making it more likely to reach the threshold required to generate an action potential (a nerve impulse). ]
How do neurons integrate multiple signals?
Neurons receive both excitatory and inhibitory signals, and the summation of these signals determines whether an action potential occurs.
Do all neurons release the same neurotransmitter?
Each neuron releases the same neurotransmitter at all of its terminals, but the effect depends on the type of receptor present on the postsynaptic cell.
What are some key neurotransmitters and their functions?
Key neurotransmitters include: Acetylcholine (ACh) - excites skeletal muscles (muscle movement), inhibits the heart; Norepinephrine - involved in autonomic responses (stress, flight or fight); Glutamate - primary excitatory neurotransmitter in the brain (learning); GABA - primary inhibitory neurotransmitter in the brain (calming)
How do drugs affect neurotransmission?
Many drugs, including anesthetics and anti-anxiety medications like Valium, act at synapses. For example, Valium enhances GABA’s inhibitory effects, increasing its calming action in the brain.
Why must neurotransmitters have a short half-life?
If neurotransmitters remained in the synapse too long, their effects would be prolonged, preventing the postsynaptic neuron from recovering.
How are neurotransmitters removed from the synapse?
Neurotransmitters are removed by enzymatic breakdown or reuptake by transporter proteins.
details: [Diffusion:
Neurotransmitters simply drift away from the synaptic cleft, where they can no longer bind to receptors.
Reuptake:
The neurotransmitter is taken back up into the presynaptic neuron (the neuron that released it) via special transport proteins. These transporters, also known as reuptake pumps, actively pump the neurotransmitter back into the axon terminal, where it can be recycled and reused.
Enzymatic Degradation:
Enzymes within the synapse break down the neurotransmitter molecules, rendering them inactive and preventing them from binding to receptors. For example, acetylcholinesterase breaks down acetylcholine.]
What is acetylcholinesterase?
Acetylcholinesterase is an enzyme that breaks down acetylcholine in the synaptic cleft.
How does the nerve gas sarin affect neurotransmission?
Sarin inhibits acetylcholinesterase, causing excessive buildup of acetylcholine, leading to overstimulation of muscles.
How do acetylcholinesterase inhibitors help treat Alzheimer’s disease?
Milder inhibitors slow the breakdown of acetylcholine, compensating for the loss of ACh-releasing neurons in Alzheimer’s patients.
How do antidepressants like Prozac and Zoloft affect neurotransmission?
They inhibit the reuptake of serotonin, increasing its levels in the synaptic cleft.
How does cocaine affect neurotransmission?
Cocaine blocks the reuptake of dopamine, causing an accumulation in the synapse and producing euphoria.
What happens to mice that lack the dopamine transporter (DAT)?
These genetically engineered mice behave similarly to normal mice given cocaine or amphetamines, as they cannot clear dopamine from the synapse. [details: (DAT) is a protein located on the plasma membrane of neurons that plays a crucial role in the regulation of dopamine neurotransmission. DAT transports dopamine (DA), a neurotransmitter, from the extracellular space back into the presynaptic neuron.]
How do amphetamines alter dopamine activity?
Amphetamines stimulate excessive dopamine release and inhibit dopamine reuptake.
How do antipsychotic drugs work?
Antipsychotic drugs block dopamine receptors on postsynaptic neurons, helping to treat disorders like schizophrenia.
How does THC affect neurotransmission?
THC (marijuana) binds to cannabinoid receptors on presynaptic neurons, reducing neurotransmitter release.
What are endocannabinoids?
Endocannabinoids are compounds produced by postsynaptic neurons that regulate neurotransmission.
Where are CB1 receptors located, and how do they explain marijuana’s effects?
- Hippocampus → Affects memory.
- Cerebellum → Impairs motor coordination.
- Hypothalamus → Increases appetite.
details: [CB1 receptors are a type of G protein-coupled receptor found primarily in the central nervous system (brain and spinal cord). They are part of the endocannabinoid system, which plays a role in regulating various physiological processes, including:
Appetite, Pain perception, Memory, Motor control, Mood, and Sleep.
When activated by cannabinoids, such as those found in cannabis (marijuana), CB1 receptors can produce a range of effects, depending on the dose and specific receptor subtype involved.]
What is synaptic plasticity?
Synaptic plasticity refers to the ability of synapses to change in strength over time.
[helpful info for context, NOT ESSENTIAL: Long-term potentiation (LTP):
When two neurons fire together frequently, the connection between them becomes stronger. This is thought to be a mechanism underlying memory formation.
Long-term depression (LTD):
Conversely, if two neurons fire together infrequently, the connection between them weakens. This may be involved in forgetting or removing unnecessary connections. ]
Why is synaptic plasticity important?
It plays a crucial role in dynamic information processing in the nervous system.
What does the impairment of motor coordination indicate?
It indicates a potential issue with the hypothalamus.
What effect does the hypothalamus have on appetite?
It increases appetite.
How was CB1 receptor research used in weight-loss drug development?
Scientists developed Acomplia, a drug that blocked CB1 receptors to suppress appetite. However, it was later removed from the market due to negative side effects.
What is synaptic plasticity?
Synaptic plasticity refers to the ability of synapses to change in strength over time, allowing for dynamic information processing in the nervous system.
Why is synaptic plasticity important?
It plays a crucial role in learning, memory formation, and brain development, especially during infancy and childhood.
What is long-term potentiation (LTP)?
LTP is a process in which repeated stimulation of a neuron strengthens the synapses, making them more effective at transmitting signals.
Where is LTP most commonly studied, and why?
LTP is primarily studied in the hippocampus, a brain region essential for learning and short-term memory.
What neurotransmitter and receptor are involved in LTP?
LTP involves the neurotransmitter glutamate, which binds to NMDA receptors on the postsynaptic neuron.
How does NMDA receptor activation contribute to synaptic strengthening?
When glutamate binds to NMDA receptors, they open channels that allow Ca²⁺ ions to enter the postsynaptic neuron, triggering biochemical changes that enhance synaptic strength.
What happens to synapses that undergo LTP?
They become more sensitive and can produce stronger responses even to weaker stimuli, helping encode new memories.
details: [Synapses that undergo long-term potentiation (LTP) become stronger, meaning they require less stimulation to produce a postsynaptic response, and this strengthening can last for hours or even days.]
What is the effect of blocking LTP?
Blocking LTP, such as by inhibiting NMDA receptors, significantly impairs learning and memory in laboratory animals.
What neurological disorders are linked to synaptic dysfunction?
Conditions such as myasthenia gravis, Parkinson’s disease, schizophrenia, and depression are associated with problems in synaptic function.
