Topic 4: chpt 8 and chpt 11 Flashcards

1
Q

What are the two parts of the nervous system?

A

-Central Nervous System (CNS): Consists of the brain and the spinal cord.

-Peripheral Nervous System (PNS): Comprises sensory (afferent) neurons and efferent neurons.

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2
Q

Describe the flow of information through the nervous system.

A

1.) Sensory Input: Sensory receptors monitor internal and external environments and send information along sensory neurons to the CNS.

2.) Integration: The CNS integrates sensory information and determines if a response is necessary.

3.) Motor Output: If a response is needed, the CNS sends output signals through efferent neurons to target muscles and glands.

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3
Q

How are efferent neurons subdivided in the nervous system?

A

-Somatic Motor Division: Controls skeletal muscles.

-Autonomic Division: Regulates smooth and cardiac muscles, exocrine glands, some endocrine glands, and some types of adipose tissue.

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4
Q

How are autonomic neurons further divided, and what distinguishes them?

A

Sympathetic and Parasympathetic Branches: Distinguished by their anatomical organization and the chemicals they use to communicate with target cells.

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5
Q

What is the enteric nervous system, and how does it function?

A

The enteric nervous system is a network of neurons in the walls of the digestive tract. It is controlled by the autonomic division but can also function autonomously as its own integrating center.

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6
Q

How are neurons classified structurally?

A

Neurons are classified structurally based on the number of processes originating from the cell body. Common structural classifications include multipolar, pseudounipolar, bipolar, and anaxonic neurons

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7
Q

Describe the structure of sensory neurons.

A

Peripheral sensory neurons are pseudounipolar, with cell bodies located close to the CNS and very long processes extending out to receptors in the limbs and internal organs. Sensory neurons in the nose and eye are smaller bipolar neurons.

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8
Q

What are interneurons, and where are they located?

A

Interneurons, also known as interconnecting neurons, lie entirely within the CNS. They have complex branching processes that allow communication with many other neurons.

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9
Q

What are the characteristics of efferent neurons?

A

Efferent neurons, both somatic motor and autonomic, typically have axons that divide into branches called collaterals and have enlarged endings called axon terminals. Many autonomic neurons also have enlarged regions along the axon called varicosities, which store and release neurotransmitters.

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10
Q

What are nerves, and how are they formed?

A

Nerves are cordlike fibers formed by the bundling together of the long axons of both afferent and efferent peripheral neurons with connective tissue. Nerves extend from the CNS to the targets of the component neurons

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11
Q

What are the types of nerves based on the signals they carry?

A

Nerves that carry only afferent signals are called sensory nerves, those that carry only efferent signals are called motor nerves, and those that carry signals in both directions are called mixed nerves.

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12
Q

What is the primary function of the cell body (cell soma) of a neuron?

A

The cell body contains DNA that serves as the template for protein synthesis, essential for the well-being of the cell.

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13
Q

Describe the structure and function of dendrites in neurons.

A

Dendrites are thin, branched processes that receive incoming information from neighboring cells. They increase the surface area of a neuron, allowing it to receive communication from multiple other neurons. Dendritic spines on dendrites can function as independent compartments and change their size and shape in response to input from neighboring cells.

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14
Q

What is the function of axons in neurons?

A

The primary function of an axon is to transmit outgoing electrical signals from the integrating center of the neuron to target cells at the end of the axon.

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15
Q

What is axonal transport, and how does it occur?

A

Axonal transport is the process by which proteins synthesized in the cell body are moved in vesicles down the axon to the axon terminal. It occurs through the action of motor proteins (kinesin-1 and dynein) that “walk” along stationary microtubules as tracks, powered by ATP.

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16
Q

How is axonal transport classified based on the speed of material movement?

A

Axonal transport is classified into fast and slow transport. Fast axonal transport moves material in both directions at rates of up to 400 mm per day, while slow axonal transport moves soluble proteins and cytoskeleton proteins at rates of 0.2–8 mm/day.

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17
Q

What are the implications of mutations or alterations in proteins associated with axonal transport?

A

Mutations or alterations in proteins associated with axonal transport have been linked to various inherited and acquired disorders, including microcephaly, fragile X syndrome, Alzheimer’s disease, and other neurodegenerative diseases.

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18
Q

What is a synapse, and what are its components?

A

A synapse is the region where an axon terminal meets its target cell. The presynaptic cell delivers a signal to the synapse, while the postsynaptic cell receives the signal. The narrow space between the two cells is called the synaptic cleft, filled with extracellular matrix fibers holding the cells in position.

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19
Q

Describe the difference between chemical and electrical synapses.

A

Chemical synapses involve the release of a chemical signal from the presynaptic cell, which diffuses across the synaptic cleft and binds to a receptor on the postsynaptic cell. Electrical synapses allow electrical current and chemical signals to pass directly between cells through gap junction channels, enabling bidirectional communication and faster signaling.

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20
Q

How do embryonic nerve cells find their correct targets and form synapses during development?

A

Embryonic nerve cells send out growth cones, special tips of axons that extend through the extracellular compartment until they find their target cell. Growth cones depend on various signals, including growth factors, molecules in the extracellular matrix, and membrane proteins, to guide them to their targets.

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21
Q

What is the significance of neurotrophic factors in the formation and maintenance of synapses?

A

Neurotrophic factors, secreted by neurons and glial cells, play a crucial role in the survival of neuronal pathways. Without electrical and chemical activity following synapse formation, the synapse may disappear. Neurotrophic factors ensure the survival of synapses and promote brain growth and development.

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22
Q

How does synaptic rearrangement occur throughout life, and why is it important?

A

Variations in electrical activity can cause rearrangement of synaptic connections, a process that continues throughout life. This synaptic plasticity allows for adaptation to changing environments and experiences. Maintaining synapses through learning new skills and information is essential for cognitive function and brain health throughout life.

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23
Q

What are glial cells, and what is their role in the nervous system?

A

Glial cells, also known as glia or neuroglia, outnumber neurons by 10–50 to 1 and provide important biochemical and structural support in the nervous system. They wrap around neurons to create structural stability, support, and insulation. Glial cells also communicate with neurons and with each other, influencing information processing and neural function.

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24
Q

Describe the function of Schwann cells and oligodendrocytes in the nervous system.

A

Schwann cells in the peripheral nervous system (PNS) and oligodendrocytes in the central nervous system (CNS) support and insulate axons by forming myelin, a substance composed of multiple concentric layers of phospholipid membrane. Myelin acts as insulation around axons and speeds up signal transmission. Schwann cells associate with one axon in the PNS, while oligodendrocytes branch and form myelin around portions of several axons in the CNS.

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25
Q

What are the nodes of Ranvier, and what role do they play in signal transmission along axons?

A

The nodes of Ranvier are tiny gaps between myelin-insulated segments of axons in the peripheral nervous system (PNS). At the nodes, a small section of axon membrane remains in direct contact with the extracellular fluid. These nodes play an important role in the transmission of electrical signals along the axon by allowing the signal to “jump” from node to node, a process known as saltatory conduction.

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26
Q

What are satellite cells, and where are they found in the nervous system?

A

Satellite cells are a type of nonmyelinating Schwann cell found in the peripheral nervous system (PNS). They form supportive capsules around nerve cell bodies located in ganglia, which are collections of nerve cell bodies found outside the central nervous system (CNS).

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27
Q

Describe the functions of astrocytes, microglia, and ependymal cells in the nervous system.

A
  • Astrocytes are highly branched CNS glial cells that provide structural support and form a functional network. They are closely associated with synapses, provide metabolic substrates for ATP production, help maintain homeostasis in the CNS extracellular fluid, and contribute to the blood-brain barrier.

-Microglia are specialized immune cells that reside permanently in the CNS. They remove damaged cells and foreign invaders but can also release damaging reactive oxygen species when activated, contributing to neurodegenerative diseases.

-Ependymal cells create a selectively permeable epithelial layer, the ependyma, that separates the fluid compartments of the CNS. They are a source of neural stem cells and contribute to the maintenance and repair of the nervous system.

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28
Q

What happens when adult neurons are injured, and how do mature neurons respond to injury?

A

When adult neurons are injured, the responses are similar to the growth of neurons during development. If the cell body dies, the entire neuron dies, but if only the axon is severed, the cell body and attached segment of axon survive. Cellular events following neuron damage include leakage of axon cytoplasm, swelling of the attached axon segment, signaling from Schwann cells to the cell body, cessation of synaptic transmission, and eventual clearance of debris by scavenger cells.

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29
Q

Describe the process of axon regeneration in the peripheral nervous system (PNS).

A

In the PNS, axons can regenerate under certain conditions. Schwann cells secrete neurotrophic factors that keep the cell body alive and stimulate axon regrowth. The regenerating axon tip behaves like a growth cone, following chemical signals in the extracellular matrix until it forms a new synapse with its target cell. However, regeneration is not always successful, and permanent loss of the axon and its pathway may occur.

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30
Q

Why is axon regeneration less likely to occur naturally in the central nervous system (CNS)?

A

In the CNS, glial cells tend to seal off and scar the damaged region, and damaged CNS cells secrete factors that inhibit axon regrowth. This inhibitory environment makes axon regeneration less likely to occur naturally in the CNS compared to the PNS.

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31
Q

How do neural stem cells contribute to neuron replacement and repair in the nervous system?

A

Neural stem cells, located in specific areas of the brain such as the hippocampus and lateral ventricle walls, remain unspecialized until they receive signals to replace damaged cells. When activated, neural stem cells transform into neurons and glial cells, contributing to neuron replacement and repair. Researchers are studying ways to control this transformation to develop treatments for injuries and degenerative neurological diseases.

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32
Q

What distinguishes nerve and muscle cells as excitable tissues?

A

They propagate electrical signals rapidly in response to stimuli, generating electrical signals for intracellular processes and communication over long distances.

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33
Q

What is the purpose of the Nernst Equation in the context of membrane potential?

A

It predicts the membrane potential for an individual ion (E_ion), based on the ion’s concentration gradient across the cell membrane, using the equation E_ion = (61/z) * log([ion]_out/[ion]_in).

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34
Q

What two factors influence the resting membrane potential according to the Nernst Equation?

A
  1. The uneven distribution of ions, particularly Na+, K+, Cl-, and Ca2+ across the cell membrane.
  2. The membrane’s permeability, with K+ having the most significant effect because the membrane is more permeable to K+ than Na+ or Ca2+.
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35
Q

How does the GHK (Goldman-Hodgkin-Katz) equation provide a more comprehensive prediction of membrane potential than the Nernst equation?

A

The GHK equation considers the contribution of all ions that can cross the membrane, incorporating their relative permeabilities, not just a single ion like the Nernst equation.

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36
Q

What is the full formula of the GHK equation? (for NA, K and CL)

A

The formula is V_m = 61 * log((P_K[K+]_out + P_Na[Na+]_out + P_Cl[Cl-]_in) / (P_K[K+]_in + P_Na[Na+]_in + P_Cl[Cl-]_out)),

-where V_m represents the membrane potential and P_ion symbolizes the relative permeability of the membrane to the ion.

-it can be simplified into words to say: Resting membrane potential (V m ) is determined by the combined contributions of the (concentration gradient * membrane permeability) for each ion.

-The GHK equation explains how the cell’s slight permeability to Na + makes the resting membrane potential more positive than the Ek determined with the Nernst equation.

-The GHK equation can also be used to predict what happens to membrane potential when ion concentrations or membrane permeabilities change.

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37
Q

What primarily determines the resting membrane potential of living cells?

A

The resting membrane potential is determined primarily by the permeability to potassium (K+), the concentration gradient of K+, and the resting permeabilities to sodium (Na+) and chloride (Cl-).

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38
Q

How do changes in K+ concentration gradient or ion permeabilities affect membrane potential?

A

Any change in the K+ concentration gradient or the permeabilities of ions like Na+ and Cl- can alter the membrane potential.

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39
Q

How is the GHK equation used to calculate changes in membrane potential?

A

The Goldman-Hodgkin-Katz (GHK) equation calculates the membrane potential by using numerical values for ion concentrations and permeabilities, allowing prediction of changes in membrane potential.

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40
Q

What happens when the membrane’s permeability to Na+ increases suddenly?

A

An increase in Na+ permeability allows Na+ to enter the cell, moving down its electrochemical gradient and depolarizing the membrane, thereby creating an electrical signal.

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41
Q

What causes a cell to hyperpolarize or depolarize?

A

Hyperpolarization occurs when the cell becomes more negative than the resting potential, and depolarization occurs when it becomes less negative (more positive).

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42
Q

Does a change in membrane potential from -70 mV to +30 mV indicate a reversal of ion concentration gradients?

A

No, a significant change in membrane potential does not imply that ion concentration gradients have reversed. Even a large change in membrane potential involves the movement of very few ions relative to total ion concentration.

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43
Q

How many ions need to move to change the membrane potential significantly?

A

To change the membrane potential by 100 mV, only about 1 out of every 100,000 K+ ions needs to move, which is a tiny fraction that does not significantly alter the overall ion concentration within the cell.

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44
Q

What are the primary ways a cell can change its ion permeability?

A

Cells can alter ion permeability by opening or closing existing channels or by adjusting the number of channels in the membrane, either by inserting new channels or removing existing ones.

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45
Q

What are the four major types of selective ion channels found in neurons?

A

Neurons contain selective ion channels specifically for Na+ (sodium), K+ (potassium), Ca2+ (calcium), and Cl- (chloride). Each type is named for the primary ion it transports.

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46
Q

What are monovalent cation channels, and how are they different from selective ion channels?

A

Monovalent cation channels are less selective and can allow both Na+ and K+ to pass through, unlike the selective channels that are specific to one type of ion.

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47
Q

What does channel conductance refer to, and how does it vary?

A

Channel conductance (G) refers to the ease with which ions flow through a channel. It varies with the gating state of the channel and the specific isoform of the channel protein.

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48
Q

What are the three main categories of gated channels found in neurons?

A
  1. Mechanically gated ion channels: Open in response to physical forces like pressure or stretch.
  2. Chemically gated ion channels: Respond to extracellular neurotransmitters and neuromodulators, or intracellular signal molecules.
  3. Voltage-gated ion channels: Open and close in response to changes in membrane potential.
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49
Q

How do voltage-gated Na+ and K+ channels contribute to neural signaling?

A

Voltage-gated Na+ channels open very rapidly upon depolarization, allowing Na+ to flow into the neuron, while K+ channels, which open more slowly, allow K+ to flow out during repolarization. This sequence supports the initiation and propagation of electrical signals along the axon.

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50
Q

What is channel inactivation, and how is it different from regular gating?

A

Channel inactivation occurs when a channel “times out” and closes automatically, despite the presence of the activating stimulus. This mechanism is different from regular gating, which depends directly on changes in membrane potential. An inactivated channel returns to its normal closed state shortly after the membrane repolarizes. The specific mechanisms underlying channel inactivation vary with different channel types

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51
Q

Discuss the diversity and modulation mechanisms of ion channels

A

Ion channels have multiple subtypes and isoforms that differ in their opening and closing kinetics and are often associated with proteins that modify their properties. Channel activity can also be modulated by chemical factors such as phosphate groups, altering how they respond to stimuli.

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52
Q

State Ohm’s law and its relevance to current flow in biological systems

A

Ohm’s law states that current flow (I) is directly proportional to the electrical potential difference (V) between two points and inversely proportional to the resistance (R) of the system to current flow, expressed as: 𝐼 = 𝑉/𝑅

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53
Q

Describe the typical movement patterns of K+, Na+, Cl-, and Ca2+ ions and their effects on the cell.

A

K+ ions usually exit the cell, leading to hyperpolarization. In contrast, Na+, Cl-, and Ca2+ usually enter the cell, often resulting in depolarization. These movements affect the cell’s membrane potential, either exciting or inhibiting cellular activity depending on the direction and magnitude of ion flow.

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54
Q

What is the impact of Na+ and K+ movement on membrane potential?

A

Influx of Na+ depolarizes the cell membrane, while K+ efflux hyperpolarizes it. The differential permeability to these ions influences the resting membrane potential.

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55
Q

What role does the Na+/K+ pump play in membrane potential?

A

The Na+/K+ pump helps maintain the resting membrane potential by moving 3 Na+ out of the cell and 2 K+ into the cell against their concentration gradients, using ATP for energy.

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56
Q

What are the three phases of an action potential?

A

The three phases of an action potential are the rising phase (depolarization), the peak (overshoot), and the falling phase (repolarization), followed by after-hyperpolarization.

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57
Q

How do graded potentials differ in the way they change membrane potential?

A

Graded potentials can be either depolarizations or hyperpolarizations and their amplitude depends on the strength of the stimulus. They decrease in strength as they spread through the cell

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58
Q

What is the initial segment in the context of action potential generation?

A

The initial segment, often found at the axon hillock, is where the action potential is typically initiated due to a high concentration of voltage-gated Na+ channels.

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59
Q

Explain the difference between conductance and conduction in neurons.

A

Conductance refers to the ability of ions to flow through channels, while conduction refers to the transmission of electrical signals along the axon.

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60
Q

Describe the term “current leak.”

A

Current leak refers to the flow of ions through the neuron cell body’s open leak channels, allowing some ions to leak out into the extracellular fluid.

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61
Q

Explain the term ‘multiplicity of form’ in the context of channel proteins.

A

Channel proteins have multiple subtypes and variants, which can express different gating and conductance behaviors known as ‘multiplicity of form.’

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62
Q

How do graded potentials reflect stimulus strength?

A

Graded potentials vary in amplitude according to the strength of the stimulus, with larger stimuli producing stronger depolarizations or hyperpolarisations.

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63
Q

Differentiate between graded potentials and action potentials.

A

Graded potentials have variable amplitude and occur mainly in dendrites and cell bodies, while action potentials have a consistent amplitude and propagate along axons.

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64
Q

What initiates the signal for graded potentials and action potentials?

A

Graded potentials are initiated by the entry of ions through gated channels, whereas action potentials are initiated by graded potentials that reach a threshold at the trigger zone.

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65
Q

Unique characteristics of graded potentials vs. action potentials.

A

Graded potentials have no minimum level required to initiate and can summate, while action potentials follow an all-or-none principle and cannot summate during the refractory period.

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66
Q

Describe the role of the absolute refractory period in action potential propagation.

A

The absolute refractory period occurs when the voltage-gated Na+ channels are either open or inactivated, making it impossible to initiate another action potential. This period ensures the unidirectional flow of the action potential along the axon and sets a limit on the frequency of action potentials.

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67
Q

What are the main sources of resistance to current flow in biological electricity?

A

The main sources of resistance to current flow in biological electricity are the resistance of the cell membrane (Rm) and the internal resistance of the cytoplasm (Ri). The resistance from the extracellular fluid (Ro) is usually negligible compared to Rm and Ri.

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68
Q

How does the opening of ion channels affect membrane resistance?

A

The opening of ion channels decreases membrane resistance. When ion channels open, ions (current) flow across the membrane if there is an electrochemical gradient for them, leading to a decrease in membrane resistance.

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69
Q

What determines the internal resistance of most neurons?

A

The internal resistance of most neurons is determined by the composition of the cytoplasm and the diameter of the cell. While cytoplasmic composition is relatively constant, internal resistance decreases as cell diameter increases. Therefore, larger diameter neurons have lower resistance.

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70
Q

What is the length constant in biological electricity, and how is it determined?

A

The length constant, sometimes called the space constant, is a measure of how far current will flow through a neuron before the energy is dissipated and the current dies. It is determined by the combination of resistances (Rm, Ri, and Ro) and can be calculated mathematically. The length constant is influenced by membrane resistance, internal resistance, and extracellular resistance.

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71
Q

What determines the strength of the initial depolarization in a graded potential?

A

The strength of the initial depolarization in a graded potential is determined by the amount of charge that enters the cell, similar to how the size of waves from a thrown stone depends on the stone’s size.

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72
Q

Why do graded potentials lose strength as they move through the cytoplasm?

A

Graded potentials lose strength due to two factors: current leak (where positive charge leaks out into the extracellular fluid) and cytoplasmic resistance (which resists the flow of electricity).

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73
Q

What is the trigger zone in a neuron?

A

The trigger zone is the integrating center of the neuron, located at the axon hillock or the initial segment of the axon in efferent neurons and interneurons, and next to the receptor in sensory neurons. It contains a high concentration of voltage-gated Na+ channels.

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74
Q

What happens when a graded potential reaches the trigger zone?

A

If a graded potential reaching the trigger zone depolarizes the membrane to the threshold voltage, voltage-gated Na+ channels open, starting an action potential. If it doesn’t reach the threshold, the potential dies out.

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75
Q

What are excitatory and inhibitory graded potentials?

A

Excitatory graded potentials make a neuron more likely to fire an action potential by depolarizing it, while inhibitory potentials make it less likely by hyperpolarizing it.

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76
Q

What is the difference between subthreshold and suprathreshold graded potentials?

A

Subthreshold graded potentials are below the threshold at the trigger zone and do not initiate an action potential, while suprathreshold graded potentials are strong enough to exceed the threshold and initiate an action potential.

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77
Q

What is neuronal excitability?

A

Neuronal excitability is the ability of a neuron to respond to a stimulus and potentially fire an action potential.

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78
Q

What are action potentials?

A

Action potentials, also known as spikes, are uniform-strength electrical signals that travel from a neuron’s trigger zone to the end of its axon without losing strength.

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79
Q

How do action potentials maintain their strength along the axon?

A

In action potentials, voltage-gated ion channels open sequentially along the axon, allowing additional Na+ to enter and reinforce the depolarization, ensuring the action potential does not lose strength over distance.

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80
Q

What is the amplitude of depolarization in an action potential?

A

The depolarization in an action potential is about 100 mV in amplitude, remaining constant along the axon from start to end.

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81
Q

What is meant by the “conduction” of an action potential?

A

The conduction of an action potential refers to the high-speed movement of this electrical signal along the axon.

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82
Q

How are action potentials described in terms of occurrence?

A

Action potentials are described as “all-or-none” phenomena—they either occur fully as a maximal depolarization if the stimulus reaches threshold or not at all if it’s below threshold.

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83
Q

Does the strength of the initiating graded potential affect the amplitude of the action potential?

A

No, the strength of the graded potential that initiates an action potential does not influence the amplitude of the action potential.

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84
Q

How does an action potential propagate along the axon?

A

Action potentials propagate along the axon like a series of falling dominos, where each segment of the axon sequentially depolarizes and repolarizes, maintaining the energy state along the axon.

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85
Q

What would recording electrodes show if placed along the axon during an action potential?

A

Recording electrodes would show overlapping action potentials at different stages along the axon, similar to dominos captured in different positions of falling.

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86
Q

What initiates an action potential in a neuron’s axon?

A

An action potential is initiated when a suprathreshold stimulus at the trigger zone depolarizes the membrane to the threshold (around -55 mV), causing voltage-gated Na+ channels to open.

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87
Q

What changes occur in the axon membrane during an action potential?

A

During an action potential, voltage-gated Na+ channels open increasing Na+ permeability, followed by the opening of K+ channels which increase K+ permeability. This sequence supports the phases of depolarization and repolarization.

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88
Q

What are the three phases of an action potential?

A

The three phases of an action potential are: 1) Rising phase (depolarization due to Na+ influx), 2) Falling phase (repolarization due to K+ efflux), 3) After-hyperpolarization phase (undershoot due to continued K+ outflow).

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89
Q

Describe the rising phase of the action potential.

A

In the rising phase, the permeability of Na+ dramatically increases due to voltage-gated Na+ channels opening. Na+ flows into the cell, driven by both concentration and electrical gradients, causing the membrane potential to rise rapidly and even reverse polarity momentarily.

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90
Q

What happens during the falling phase of an action potential?

A

During the falling phase, voltage-gated K+ channels open (slower than Na+ channels) as Na+ channels close. K+ moves out of the cell, driven by its concentration and electrical gradients, rapidly bringing the membrane potential back towards the resting level.

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91
Q

What is the after-hyperpolarization phase?

A

After-hyperpolarization, or undershoot, occurs when the membrane potential dips below the normal resting potential due to continued K+ efflux, even as K+ permeability begins to decrease and the cell approaches the K+ equilibrium potential.

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92
Q

How does the neuron return to resting membrane potential after an action potential?

A

After the action potential, slow voltage-gated K+ channels close, and the leak of ions through channels slowly returns the membrane potential to -70 mV, the resting state determined by permeability to K+, Cl-, and Na+.

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93
Q

What contributions did A.L. Hodgkin and A.F. Huxley make regarding action potentials?

A

A.L. Hodgkin and A.F. Huxley described the mechanism of action potentials in neurons and won the Nobel Prize in 1963 for their work detailing how voltage-gated ion channels contribute to neuronal signaling.

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94
Q

How many action potentials could a neuron fire before its ion gradients are significantly altered if the Na+ K+ pump were non-functional?

A

A neuron without a functional Na+ K+ pump could fire a thousand or more action potentials before a significant change in the ion gradients occurred.

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95
Q

What are the two gates of a voltage-gated Na+ channel and their roles?

A

Voltage-gated Na+ channels have two gates: the activation gate and the inactivation gate. The activation gate opens in response to depolarization allowing Na+ to enter the cell, while the inactivation gate, which delays closing, eventually stops Na+ influx to end the action potential.

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96
Q

How do the activation and inactivation gates of Na+ channels function during an action potential?

A

Upon depolarization, the activation gate quickly opens allowing Na+ in, further depolarizing the cell. The inactivation gate then closes after a delay of 0.5 msec, stopping Na+ entry and leading to the peak of the action potential.

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97
Q

What happens to Na+ channels after the action potential peaks?

A

After the action potential peaks, as the cell repolarizes due to K+ efflux, the Na+ channel gates reset to their original positions, with the activation gate closing and the inactivation gate opening, preparing for the next potential depolarization.

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98
Q

How does the double-gating mechanism of Na+ channels influence the directionality of electrical signals in neurons?

A

The double-gating mechanism ensures that electrical signals in neurons are conducted in only one direction, a feature further explored in subsequent sections of the neuron study.

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99
Q

What is the refractory period in the context of neuron action potentials?

A

The refractory period is the time during which a neuron cannot trigger a second action potential, no matter how strong the incoming stimulus is. This period ensures that action potentials are unidirectional and do not overlap.

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100
Q

What is the absolute refractory period?

A

The absolute refractory period is the time after an action potential begins during which no second action potential can be triggered, typically lasting about 1–2 msec. This is the time required for the Na+ channel gates to reset to their resting positions.

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101
Q

How does the absolute refractory period affect the directionality of action potentials?

A

Due to the absolute refractory period, action potentials cannot overlap and cannot travel backward, ensuring they move from the trigger zone to the axon terminal in a controlled manner.

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102
Q

What is the relative refractory period?

A

Following the absolute refractory period, the relative refractory period is when some Na+ channels have reset, but not all. A stronger-than-normal stimulus is required to trigger another action potential during this period.

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103
Q

How does the relative refractory period affect action potential amplitude?

A

During the relative refractory period, action potentials that do occur may have a smaller amplitude than normal. This is due to some Na+ channels still being inactive and simultaneous K+ efflux, which opposes depolarization.

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104
Q

How do refractory periods differ between action potentials and graded potentials?

A

Unlike action potentials, graded potentials can summate if they occur close in time. During the absolute refractory period, even suprathreshold graded potentials have no effect on triggering an action potential, as the Na+ channels are inactivated.

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105
Q

How do refractory periods affect signal transmission in neurons and ensure the directionality of action potentials?

A

Refractory periods limit the rate at which neurons can transmit signals by preventing a new action potential from starting too soon after the previous one. The absolute refractory period ensures that action potentials travel in only one direction—from the cell body to the axon terminal—by preventing backward travel of the action potential. This is crucial for the proper functioning of neural circuits and signal propagation

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106
Q

How does the conduction of an action potential occur at the cellular level?

A

Conduction occurs when depolarization of a section of axon causes local current flow in the cytoplasm and back toward the depolarized section from the outside of the axon. Voltage-gated Na+ channels open in response to depolarization, allowing Na+ to enter, reinforcing the depolarization and maintaining the strength of the action potential.

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107
Q

What role do voltage-gated Na+ channels play in action potential conduction?

A

Voltage-gated Na+ channels play a crucial role in action potential conduction by opening in response to depolarization, allowing more Na+ to enter the cell. This positive feedback loop ensures continuous depolarization along the axon, preventing the signal from diminishing.

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108
Q

How does the action potential prevent signal loss as it travels down the axon?

A

As the action potential propagates, each axonal segment depolarizes sequentially due to local current flow and the opening of Na+ channels. This results in a continuous entry of Na+ that keeps the action potential’s strength constant.

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109
Q

What prevents the action potential from moving backward along the axon?

A

The absolute refractory period prevents backward movement of the action potential. After an action potential, Na+ channels inactivate, making it impossible for the action potential to move backward, ensuring one-way signal propagation

110
Q

What are the two key physical parameters that influence the speed of action potential conduction in a neuron?

A

The two key parameters are (1) the diameter of the axon and (2) the resistance of the axon membrane to ion leakage, known as the length constant. Larger axon diameters and more leak-resistant membranes result in faster conduction speeds.

111
Q

How does the diameter of an axon affect the speed of action potential conduction?

A

Similar to water flowing through a large-diameter pipe with less resistance, charges flowing inside a large-diameter axon encounter less resistance from the membrane. This reduced resistance allows for faster action potential conduction.

112
Q

How does myelination affect the speed of action potential conduction in axons?

A

Myelination increases the speed of action potential conduction by insulating the axon with myelin sheaths, reducing current leak and allowing action potentials to leap from node to node (nodes of Ranvier), where ion channels are concentrated. This saltatory conduction is much faster than the continuous conduction in unmyelinated axons.

113
Q

What is saltatory conduction and how does it work?

A

Saltatory conduction is the rapid transmission of action potentials in myelinated axons, where the action potential “jumps” from one node of Ranvier to the next. This occurs because the myelin sheath insulates the axon segments between nodes, preventing ion leakage and speeding up neural signaling

114
Q

What are the effects of demyelinating diseases on neural conduction?

A

Demyelinating diseases, such as Multiple Sclerosis and Guillain-Barré syndrome, result in the loss of myelin, which slows down action potential conduction. This slowing can cause the depolarization reaching the nodes of Ranvier to fall below the threshold needed for action potential propagation, leading to a variety of neurological symptoms.

115
Q

What are the effects of altered extracellular K+ and Ca2+ concentrations on neuron activity?

A

Changes in extracellular K+ and Ca2+ levels can lead to abnormal electrical activity in the nervous system. For K+, variations from the normal range significantly impact the resting membrane potential and thus the excitability of nerve and muscle cells.

116
Q

What is hyperkalemia and how does it affect neuronal function?

A

Hyperkalemia is an increase in blood K+ concentration, which shifts the resting membrane potential of neurons closer to the threshold, making cells more likely to fire action potentials in response to smaller graded potentials.

117
Q

What is hypokalemia and its impact on neuronal and muscular function?

A

Hypokalemia is a decrease in blood K+ concentration, leading to hyperpolarization of the resting membrane potential and moving it farther from the threshold. This results in muscle weakness as neurons controlling skeletal muscles do not fire normally.

118
Q

What is the role of potassium homeostasis in the nervous system?

A

Potassium homeostasis mechanisms are crucial as they maintain blood K+ concentrations within a narrow range, essential for the normal function of the nervous system and preventing conditions like hyperkalemia and hypokalemia.

119
Q

What are the two parts of a synapse?

A

Each synapse consists of two parts: (1) the axon terminal of the presynaptic cell, and (2) the membrane of the postsynaptic cell.

120
Q

What types of cells can be postsynaptic cells in neuron-to-neuron synapses?

A

Postsynaptic cells can be either neurons or non-neuronal cells. In neuron-to-neuron synapses, the presynaptic axon terminals are typically next to the dendrites or cell body of the postsynaptic neuron.

121
Q

How prevalent are synapses on postsynaptic neurons with many dendrites?

A

Postsynaptic neurons with many dendrites generally have many synapses. A moderate number of synapses is around 10,000, but some brain cells may have up to 150,000 synapses on their dendrites.

122
Q

What are the two main types of synapses?

A

Synapses are classified as either electrical or chemical. Electrical synapses pass an electrical signal directly between cells, while chemical synapses use neurocrine molecules to transfer information across a synaptic cleft.

123
Q

What are electrical synapses and where are they found?

A

Electrical synapses allow direct passage of an electrical signal between cells through gap junctions. They are found mainly in the CNS neurons, glial cells, cardiac and smooth muscle, and some nonexcitable cells like pancreatic beta cells.

124
Q

What is the primary advantage of electrical synapses?

A

The primary advantage of electrical synapses is the rapid and bidirectional conduction of signals, which helps synchronize activity within a network of cells. Gap junctions also permit the diffusion of chemical signals between cells.

125
Q

How do chemical synapses transmit signals?

A

In chemical synapses, the electrical signal from the presynaptic cell is converted into a neurocrine signal that crosses the synaptic cleft and binds to receptors on the postsynaptic cell, thereby transferring information.

126
Q

What are the three types of neurocrine molecules and their functions?

A

Neurocrine molecules function as neurotransmitters, neuromodulators, or neurohormones. Neurotransmitters act as paracrine signals at synapses for rapid responses. Neuromodulators can act both synaptically and non-synaptically and are slower-acting. Neurohormones are secreted into the blood and affect distant targets throughout the body.

127
Q

How are neurotransmitters and neuromodulators distinguished?

A

The distinction is based on the receptor to which they bind and their speed of action. Neurotransmitters elicit rapid responses at synapses, while neuromodulators act more slowly and at both synaptic and nonsynaptic sites. Many neurocrine molecules can act as both.

128
Q

What are the two types of neurocrine receptors?

A

Neurocrine receptors are categorized into receptor-channels (ionotropic receptors) and G protein-coupled receptors (metabotropic receptors). Ionotropic receptors mediate rapid responses by altering ion flow, while metabotropic receptors mediate slower responses through second messengers.

129
Q

What are the specificities of ionotropic receptors?

A

Some ionotropic receptors are specific to a single type of ion, such as Cl-, while others like the nonspecific monovalent cation channel allow both Na+ and K+ to pass through.

130
Q

How do G protein-coupled receptors function?

A

G protein-coupled receptors (GPCRs) mediate slower responses through a second messenger system. Some GPCRs regulate ion channels, affecting cellular responses over a longer duration.

131
Q

What role do agonists and antagonists play in neurotransmitter research?

A

Agonists and antagonists are crucial in neurotransmitter research as they mimic or inhibit neurotransmitter activity by binding to their receptors. This allows for detailed study of neurotransmitter functions and receptor interactions.

132
Q

What are the seven classes of neurocrine molecules according to their structure?

A

The seven classes of neurocrine molecules are: (1) acetylcholine, (2) amines, (3) amino acids, (4) peptides, (5) purines, (6) gases, and (7) lipids.

133
Q

How is acetylcholine synthesized and what are its receptor subtypes?

A

Acetylcholine is synthesized from choline and acetyl CoA. Its receptors are categorized into nicotinic, which are ion channels affecting skeletal muscle and the nervous system, and muscarinic, which are GPCRs affecting various tissues through second messenger systems.

134
Q

What are the amine neurotransmitters and their origins?

A

Amine neurotransmitters include serotonin (from tryptophan), histamine (from histidine), dopamine, norepinephrine, and epinephrine (all three from tyrosine). They function in the CNS and PNS, with roles in neurotransmission and hormonal activity.

135
Q

Describe the neurotransmitter roles of amino acids in the CNS.

A

Glutamate is the primary excitatory neurotransmitter, while GABA is the main inhibitory neurotransmitter in the CNS. Glutamate can also act as a neuromodulator, affecting cells through ionotropic (e.g., AMPA, NMDA) and metabotropic receptors.

136
Q

What neurotransmitter roles do peptides play in the nervous system?

A

Peptides such as substance P, enkephalins, and endorphins act as neurotransmitters and neuromodulators. They are involved in pain pathways and analgesia, and some also function as neurohormones like vasopressin and atrial natriuretic peptide.

137
Q

How do purines function as neurotransmitters?

A

Purines like adenosine, AMP, and ATP act as neurotransmitters binding to purinergic GPCR receptors, affecting various systems including the CNS and heart.

138
Q

What are the roles of gas neurotransmitters like nitric oxide and carbon monoxide?

A

Gas neurotransmitters such as nitric oxide and carbon monoxide diffuse directly into target cells to modulate functions. Nitric oxide, for instance, binds to internal proteins and influences various cellular processes.

139
Q

What are lipid neurocrine molecules and their receptors?

A

Lipid neurocrines include eicosanoids, which are ligands for cannabinoid receptors CB1 and CB2. CB1 is primarily found in the brain, while CB2 is located on immune cells. These neurocrines play significant roles in various physiological processes, including those affected by exogenous ligands like THC from marijuana.

140
Q

How do nicotinic and muscarinic acetylcholine receptors differ in function and location?

A

Nicotinic acetylcholine receptors are ionotropic, primarily found on skeletal muscle and in both the CNS and autonomic division of the PNS, facilitating rapid depolarization and excitation. Muscarinic receptors are metabotropic, more diverse in function, influencing various physiological processes via G protein-coupled mechanisms and are widely distributed in the CNS and the autonomic parasympathetic system.

141
Q

What are the physiological implications of serotonin as a neurotransmitter?

A

Serotonin (5-HT), derived from tryptophan, is crucial in modulating mood, emotion, sleep, and appetite. Dysregulation of serotonin levels or receptor function is associated with depression, anxiety, and other psychiatric conditions.

142
Q

Explain the role and mechanism of GABA as the primary inhibitory neurotransmitter in the CNS.

A

GABA (gamma-aminobutyric acid) primarily functions to reduce neuronal excitability throughout the nervous system by opening Cl- channels when it binds to its receptors. This influx of Cl- ions hyperpolarizes the neuron, making it less likely to fire an action potential.

143
Q

What is the significance of glutamate in CNS neurotransmission?

A

Glutamate is the most abundant excitatory neurotransmitter in the CNS, facilitating synaptic plasticity and brain development. It operates through both ionotropic receptors (like AMPA and NMDA) that directly mediate ionic changes, and metabotropic receptors that affect neurons via second-messenger pathways.

144
Q

How do adrenergic receptors function and what are their types?

A

Adrenergic receptors, responding to norepinephrine and epinephrine, are divided into alpha (α) and beta (β) types, each with several subtypes. Alpha receptors generally cause excitatory actions like vasoconstriction, while beta receptors typically mediate inhibitory actions such as vasodilation, depending on the subtype and tissue.

145
Q

Describe the dual role of neurotransmitters such as dopamine.

A

Dopamine functions both as a neurotransmitter in the CNS, playing key roles in reward, motivation, and motor control, and as a neurohormone in the PNS. Dysregulation of dopamine pathways is implicated in disorders such as Parkinson’s disease and schizophrenia.

146
Q

What is the role of peptides like enkephalins in the nervous system?

A

Enkephalins are one of the opioid peptides that act as neurotransmitters and neuromodulators to mediate pain relief and analgesia in the nervous system. They bind to opioid receptors in the brain to reduce the perception of pain.

147
Q

Discuss the impact of purines like ATP in neurotransmission.

A

ATP and other purines act as neurotransmitters by binding to purinergic receptors, influencing a variety of physiological processes including cardiovascular function, muscle contraction, and neurotransmission. ATP is particularly significant in mediating fast synaptic transmission at both central and peripheral sites.

148
Q

What are the key sites for neurotransmitter synthesis in neurons?

A

Neurotransmitters are synthesized in both the nerve cell body and the axon terminal. Polypeptides are produced in the cell body due to the necessary organelles for protein synthesis, while smaller neurotransmitters like acetylcholine and amines are synthesized in the axon terminal.

149
Q

How are neurotransmitters stored and released in axon terminals?

A

Neurotransmitters are stored in synaptic vesicles within the axon terminal. These vesicles are docked at active zones ready for rapid release or held in reserve pools. Release occurs via exocytosis, triggered by calcium ion influx upon depolarization of the axon terminal.

150
Q

Describe the process and significance of exocytosis in neurotransmitter release.

A

Exocytosis involves the fusion of synaptic vesicle membranes with the axon terminal membrane, allowing neurotransmitters to enter the synaptic cleft. This process is crucial for neurotransmitter-mediated communication between neurons and is regulated by calcium ions and specific membrane proteins.

151
Q

What are the two models of neurotransmitter release?

A

The classic model involves the complete fusion of vesicles with the plasma membrane followed by endocytosis to recycle the membrane. The “kiss-and-run” model involves a transient opening (fusion pore) that allows neurotransmitter release without full vesicle fusion, allowing quick reuse of vesicles.

152
Q

How is neurotransmitter activity terminated in the synaptic cleft?

A

Termination of neurotransmitter activity can occur through diffusion away from the synapse, enzymatic degradation (e.g., acetylcholinesterase breaking down ACh), or reuptake into presynaptic cells or nearby glia, often involving specific transporters.

153
Q

What role do transporters play in the synaptic cleft?

A

Transporters help maintain neurotransmitter levels by reabsorbing them into the presynaptic neuron or adjacent glial cells. For example, norepinephrine and serotonin are taken up by specific Na+-dependent cotransporters, which is crucial for recycling and terminating neurotransmitter action.

154
Q

Explain the significance of neurotransmitter recycling.

A

Recycling of neurotransmitters, such as the reuptake of choline into presynaptic cells to synthesize new acetylcholine, is essential for sustaining neurotransmission and efficient neural communication, reducing the need for new synthesis and conserving cellular resources.

155
Q

How do enzymatic activities influence neurotransmitter function in the synaptic cleft?

A

Enzymes in the synaptic cleft, like acetylcholinesterase, rapidly break down neurotransmitters post-release. This enzymatic activity is critical for resetting the synaptic environment, ensuring that signals are sharp and do not linger excessively, which could lead to desensitization or continuous activation.

156
Q

How do neurons use action potentials to transmit information about stimulus duration and strength?

A

Neurons encode the duration of a stimulus by the duration of a series of action potentials. The strength of a stimulus is encoded by the frequency of action potentials; a stronger stimulus results in more action potentials per second, leading to increased neurotransmitter release at the axon terminal.

157
Q

How does a sensory neuron communicate the intensity of a stimulus to the CNS?

A

A sensory neuron communicates stimulus intensity by the number and frequency of action potentials triggered by an above-threshold graded potential. Stronger graded potentials generate more frequent action potentials, indicating a higher intensity stimulus.

158
Q

What is the relationship between action potential frequency and neurotransmitter release?

A

The frequency of action potentials affects neurotransmitter release such that higher frequencies, indicative of stronger stimuli, result in the release of more neurotransmitter from the axon terminal into the synaptic cleft.

159
Q

Describe the variability in electrical signaling patterns among CNS neurons.

A

CNS neurons display diverse electrical signaling patterns, including tonic activity with regular action potential firing and bursting patterns with rhythmic bursts interspersed with quiet intervals. These patterns are influenced by different ion channel variants, which vary in activation/inactivation thresholds, opening/closing speeds, and neuromodulator sensitivity.

160
Q

How do ion channel variants affect neuronal firing patterns in the CNS?

A

Variants in ion channels contribute to the diverse firing patterns observed in CNS neurons. These variations allow neurons to respond differently based on their electrical properties, which are shaped by the specific ion channels’ characteristics such as voltage sensitivity and reaction to neuromodulators.

161
Q

What role do bursts of action potentials play in CNS function?

A

Bursting, or the rhythmic firing of clusters of action potentials, plays a role in signal encoding within the CNS, allowing neurons to communicate complex information regarding the timing and strength of stimuli. This can influence various neural processes and behaviors.

162
Q

What is synaptic divergence and how does it function in the nervous system?

A

Synaptic divergence occurs when the axon of a presynaptic neuron branches and synapses on multiple target neurons. This pattern allows a single neuronal signal to be distributed to various parts of the nervous system, enhancing the spread and integration of neural information.

163
Q

Explain synaptic convergence in neural communication

A

Synaptic convergence involves multiple presynaptic neurons providing input to a smaller number of postsynaptic neurons. This allows integration of signals from various sources, which can modify the response of the postsynaptic neurons based on the cumulative inputs they receive.

164
Q

Describe the concept of synaptic plasticity and its types.

A

Synaptic plasticity is the ability of synapses to change their strength or efficiency in response to increases or decreases in their activity. It includes short-term changes like facilitation and depression, as well as long-term changes like long-term potentiation (LTP) and long-term depression (LTD), crucial for learning and memory.

165
Q

How do slow and fast synaptic responses differ?

A

Slow synaptic responses involve G protein-coupled receptors and second messengers, affecting cellular processes over seconds to minutes, potentially altering protein function or gene expression. Fast synaptic responses are mediated by receptor-channels that directly alter ion flow, causing rapid changes in membrane potential lasting only milliseconds.

166
Q

What are EPSPs and IPSPs, and how do they affect neuronal excitability?

A

Excitatory Postsynaptic Potentials (EPSPs) are depolarizing changes in membrane potential that increase the likelihood of a neuron firing an action potential. Inhibitory Postsynaptic Potentials (IPSPs) are hyperpolarizing changes that decrease the likelihood of action potential generation, moving the membrane potential further from the threshold.

167
Q

How does synaptic communication contribute to long-term changes in neuronal function?

A

Synaptic communication can lead to long-term changes in neuronal function through mechanisms like long-term potentiation and depression, which alter synaptic strength. These changes are linked to processes such as the growth and development of neurons and the formation of long-term memory.

168
Q

What role do neuromodulators play in synaptic communication?

A

Neuromodulators “talk back” to presynaptic neurons by binding to receptors on presynaptic cells. This feedback can influence neurotransmitter release and synaptic plasticity, adjusting the presynaptic neuron’s output in response to changing conditions.

169
Q

Discuss the impact of ion channel variants on CNS neuron firing patterns.

A

Variants in ion channels affect the activation and inactivation voltages, opening and closing speeds, and sensitivity to neuromodulators, contributing to diverse firing patterns in CNS neurons such as tonic activity and bursting. This variability allows for dynamic responses to physiological demands.

170
Q

What is spatial summation in neural communication?

A

Spatial summation occurs when multiple graded potentials from different presynaptic neurons converge on a single postsynaptic neuron. The combined effect of these potentials, which may be excitatory or inhibitory, determines whether the postsynaptic neuron reaches the threshold to fire an action potential.

171
Q

How can spatial summation lead to an action potential?

A

If multiple excitatory neurons fire simultaneously and their excitatory postsynaptic potentials (EPSPs) sum up to exceed the threshold at the postsynaptic neuron’s trigger zone, an action potential is generated. This summation reflects the integration of signals from various locations on the neuron.

172
Q

What is postsynaptic inhibition and how does it occur through spatial summation?

A

Postsynaptic inhibition occurs when the sum of inhibitory postsynaptic potentials (IPSPs) and EPSPs at a postsynaptic neuron’s trigger zone does not reach the threshold for firing an action potential. This can happen when inhibitory signals counteract the excitatory ones, preventing the neuron from firing.

173
Q

Define temporal summation and describe how it influences neuron firing.

A

Temporal summation occurs when two subthreshold graded potentials from the same or different presynaptic neurons arrive at the postsynaptic neuron’s trigger zone closely in time. The overlapping of these potentials can cumulatively reach or exceed the threshold, leading to an action potential.

174
Q

What is the difference between spatial and temporal summation?

A

Spatial summation involves graded potentials from different spatial locations on the neuron converging simultaneously, while temporal summation involves graded potentials arriving closely in time, potentially from the same location. Both processes are critical for integrating synaptic inputs.

175
Q

How do neurons integrate multiple synaptic inputs?

A

Neurons integrate synaptic inputs through mechanisms of spatial and temporal summation, considering the relative strengths and timing of incoming signals. This postsynaptic integration determines whether the neuron will fire an action potential based on whether the combined signal is above or below the threshold.

176
Q

Why is postsynaptic integration important in neural networks?

A

Postsynaptic integration allows neurons to process and respond to complex patterns of input from multiple sources. It is crucial for the regulation of neural activity, enabling the nervous system to make coordinated responses to varied stimuli

177
Q

What is presynaptic modulation and how does it affect neurotransmitter release?

A

Presynaptic modulation occurs when a modulatory neuron affects a presynaptic cell, altering its neurotransmitter release. This can enhance neurotransmitter release through presynaptic facilitation or decrease it via presynaptic inhibition, depending on whether the modulatory input is excitatory or inhibitory.

178
Q

Describe the difference between global and selective presynaptic inhibition.

A

Global presynaptic inhibition affects all axon collaterals of a neuron uniformly, reducing neurotransmitter release broadly. Selective presynaptic inhibition targets specific collaterals, allowing precise control over which postsynaptic cells are affected by the modulation.

179
Q

How can synaptic activity be altered by changes in the postsynaptic cell?

A

Synaptic activity can be altered by changing the postsynaptic cell’s responsiveness to neurotransmitters. This can involve modifications to the structure, affinity, or number of neurotransmitter receptors, often influenced by neuromodulators through second messenger systems.

180
Q

What roles do neuromodulators play in synaptic modulation?

A

Neuromodulators can alter neurotransmitter effects by influencing receptor properties and other cellular components like enzymes and transporters. Their actions, mediated through second messenger systems, typically have longer-lasting effects than neurotransmitters and can affect both presynaptic and postsynaptic activity.

181
Q

How does the dual role of certain signal molecules as neurotransmitters and neuromodulators affect neural communication?

A

Some molecules can function as both neurotransmitters and neuromodulators depending on the receptor to which they bind. As neurotransmitters, they directly activate ion channels or receptors for fast responses; as neuromodulators, they typically engage G-protein coupled receptors to initiate slower, longer-lasting, broader regulatory effects through second messenger pathways.

182
Q

What are Long-Term Potentiation (LTP) and Long-Term Depression (LTD)?

A

LTP and LTD are forms of synaptic plasticity where sustained activity at a synapse leads to long-lasting changes in the quality or quantity of synaptic connections. LTP enhances synaptic strength, while LTD reduces it, both playing critical roles in learning and memory.

183
Q

How does glutamate relate to LTP and LTD?

A

Glutamate, the main excitatory neurotransmitter in the CNS, binds to AMPA and NMDA receptors, playing a pivotal role in LTP and LTD. The interaction of glutamate with these receptors facilitates changes in synaptic strength through mechanisms of receptor activation and ion flow.

184
Q

Describe the unique properties of NMDA receptors in synaptic plasticity.

A

NMDA receptors are blocked by Mg2+ ions at resting membrane potentials. Upon depolarization and glutamate binding, Mg2+ is expelled, allowing ions like Ca2+ to flow through. This Ca2+ influx is crucial for activating intracellular pathways that lead to synaptic plasticity.

185
Q

What role does Ca2+ play in LTP?

A

In LTP, Ca2+ entry through NMDA receptors triggers second messenger pathways that enhance the postsynaptic cell’s sensitivity to glutamate. This often involves up-regulation of glutamate receptors and can also influence presynaptic neurotransmitter release.

186
Q

How does long-term depression occur at synapses?

A

LTD involves the withdrawal of AMPA receptors from the postsynaptic membrane through endocytosis, reducing synaptic strength. It can also involve changes in the subunit composition of these receptors, affecting the flow of ions and thus synaptic efficacy.

187
Q

What are the implications of LTP and LTD for neurological conditions?

A

LTP and LTD are linked to fundamental neural processes such as learning and memory. Abnormalities in these processes are associated with clinical conditions like depression and other mental illnesses, making them significant areas of neuroscience research.

188
Q

How does synaptic activity lead to changes in neurotransmitter receptor density or type?

A

Synaptic activity can lead to the insertion or removal of neurotransmitter receptors in the postsynaptic membrane, affecting receptor density and type. This modulation of receptor properties is a key mechanism by which neurons adapt their responses to sustained synaptic activity.

189
Q

How does myasthenia gravis illustrate a disorder of synaptic transmission?

A

Myasthenia gravis is a neuromuscular disorder characterized by weakness and fatigue of voluntary muscles, primarily caused by antibodies that block or destroy nicotinic acetylcholine receptors at the neuromuscular junction, impairing synaptic transmission.

190
Q

What is the efferent division of the peripheral nervous system (PNS), and what does it control?

A

The efferent division of the PNS carries commands from the central nervous system (CNS) to muscles and glands, facilitating rapid responses. It includes somatic motor neurons controlling skeletal muscles and autonomic neurons controlling smooth muscle, cardiac muscle, glands, and some adipose tissue.

191
Q

Describe the somatic and autonomic divisions of the PNS.

A

The somatic division controls voluntary movements of skeletal muscles, though it also handles some involuntary reflexes like swallowing. The autonomic division, typically involuntary, manages functions of smooth and cardiac muscles and glands, but can be influenced by biofeedback to control functions like heart rate.

192
Q

How do mixed nerves function within the PNS?

A

Mixed nerves in the PNS contain both afferent and efferent fibers, allowing them to conduct sensory information to the CNS and motor commands from the CNS to the body, enabling comprehensive neural communication.

193
Q

What are the subdivisions of the autonomic nervous system?

A

The autonomic nervous system is divided into the sympathetic and parasympathetic nervous systems. The sympathetic system prepares the body for stress (‘fight or flight’), while the parasympathetic system promotes resting functions (‘rest and digest’).

194
Q

What does the prefix “para-“ in parasympathetic imply?

A

The prefix “para-“ means beside or alongside, indicating that the parasympathetic nervous system works alongside the main functions to manage routine, calming activities like digestion.

195
Q

How do the sympathetic and parasympathetic nervous systems interact in daily activities?

A

These systems dynamically balance body functions by seesawing back and forth to regulate various physiological processes. While the parasympathetic system typically dominates during restful states, the sympathetic system can modulate specific functions like blood flow during both calm and stressful conditions.

196
Q

How is autonomic nervous system activity integrated in the body?

A

The integration of sympathetic and parasympathetic activities is crucial for maintaining homeostasis. They continuously adjust their influence over organ systems to respond to both internal conditions and external stressors, fine-tuning the body’s responses.

197
Q

How do the autonomic and endocrine systems collaborate to maintain homeostasis?

A

The autonomic nervous system and the endocrine system work together closely, with sensory information from various receptors being processed by control centers in the hypothalamus, pons, and medulla. These centers regulate vital functions such as blood pressure, temperature, and water balance, coordinating endocrine and autonomic responses to maintain homeostasis.

198
Q

What roles do the hypothalamus and brain stem play in regulating bodily functions?

A

The hypothalamus and brain stem act as homeostatic control centers, receiving sensory inputs and producing motor outputs that create autonomic, endocrine, and behavioral responses. These responses include drinking, food-seeking, and temperature regulation, crucial for survival and comfort.

199
Q

How do emotions influence autonomic responses?

A

Emotions, processed in the cerebral cortex and limbic system, can significantly influence autonomic outputs. Emotional responses, such as blushing, fainting, or feeling “butterflies in the stomach,” demonstrate the interplay between emotional states and autonomic functions.

200
Q

What is the significance of osmoreceptors and thermoreceptors in the hypothalamus?

A

Osmoreceptors and thermoreceptors in the hypothalamus monitor the body’s osmolarity and temperature, respectively. They are crucial for triggering appropriate autonomic responses to maintain fluid balance and thermal regulation.

201
Q

Describe the role of spinal reflexes in autonomic functions.

A

Spinal reflexes such as urination, defecation, and penile erection operate under autonomic control and can occur without direct brain input. These reflexes are crucial for bodily functions and can still function to a degree in individuals with spinal cord injuries, although such injuries may disrupt the ability to sense or voluntarily control these reflexes.

202
Q

How do brain centers for motivated behaviors integrate with autonomic responses?

A

Brain centers responsible for motivated behaviors, such as seeking food or regulating temperature, integrate sensory inputs and emotional states to produce coordinated movements and behaviors. These centers influence autonomic outputs to ensure that behavioral responses are aligned with the body’s physiological needs.

203
Q

What are Walter Cannon’s four properties of homeostasis as they relate to the autonomic nervous system?

A

The four properties are: (1) preservation of the fitness of the internal environment, ensuring optimal functioning of body systems; (2) up-down regulation by tonic control, allowing fine-tuned responses; (3) antagonistic control, where one branch stimulates and the other inhibits to maintain balance; (4) chemical signals having different effects in different tissues, providing targeted responses.

204
Q

How do the sympathetic and parasympathetic nervous systems regulate heart rate?

A

Heart rate is under antagonistic control: sympathetic innervation increases heart rate to prepare the body for action, while parasympathetic innervation decreases it during restful states, allowing precise regulation of cardiovascular function.

205
Q

Explain the concept of antagonistic control in the autonomic nervous system.

A

Antagonistic control involves the sympathetic and parasympathetic branches having opposite effects on the same organ to maintain homeostasis. For example, one branch may excite an organ’s function while the other inhibits it, balancing the organ’s activity as needed.

206
Q

Describe an example of cooperative control by the autonomic nervous system.

A

A cooperative control example is sexual function, where parasympathetic nerves control blood flow for penile erection, and sympathetic nerves direct muscle contraction for ejaculation, demonstrating coordinated effort for a common physiological goal

207
Q

How do adrenergic receptors affect vascular smooth muscle function?

A

In blood vessels, different types of adrenergic receptors can induce opposite effects: one type may cause vasoconstriction by contracting smooth muscle, while another causes vasodilation by relaxing it. The response is determined by the specific receptor type activated by catecholamines like norepinephrine and epinephrine.

208
Q

What is tonic control and how does it apply to certain autonomic functions?

A

Tonic control refers to the continuous regulation of an organ’s activity by varying the signal intensity. For instance, sweat glands and many blood vessels, which lack parasympathetic innervation, are regulated solely by the sympathetic nervous system’s tonic control, adjusting their activity as necessary without direct antagonistic influence.

209
Q

What are the components of an autonomic pathway?

A

Autonomic pathways consist of two neurons in a series: the preganglionic neuron that originates in the CNS and projects to an autonomic ganglion, and the postganglionic neuron, which starts at the ganglion and extends its axon to the target tissue.

210
Q

Describe the role of the preganglionic and postganglionic neurons in the autonomic nervous system.

A

The preganglionic neuron carries signals from the CNS to an autonomic ganglion, where it synapses with the postganglionic neuron. The postganglionic neuron then transmits these signals to various target tissues, executing autonomic functions.

211
Q

What is the significance of divergence in autonomic pathways?

A

Divergence in autonomic pathways allows a single preganglionic neuron to influence multiple postganglionic neurons, each of which may control different target tissues. This amplifies the effect of one CNS signal across a wide area of the body

212
Q

Explain the concept of a reflex integrated within an autonomic ganglion.

A

Some reflexes may be entirely processed within an autonomic ganglion, allowing for rapid, localized responses to stimuli without needing to relay information back and forth from the CNS. This is particularly evident in the enteric nervous system.

213
Q

How does the enteric nervous system illustrate autonomic control?

A

The enteric nervous system, part of the autonomic nervous system that governs the digestive system, operates semi-independently, handling complex reflexes locally within its own network of neurons, demonstrating advanced autonomy within the autonomic pathways.

214
Q

What neurotransmitters do preganglionic neurons in the autonomic nervous system release, and what receptors do they target?

A

Both sympathetic and parasympathetic preganglionic neurons release acetylcholine (ACh), which acts on nicotinic cholinergic receptors (nAChR) on the postganglionic neurons.

215
Q

What neurotransmitter is commonly released by sympathetic postganglionic neurons, and which receptors do they target?

A

Most sympathetic postganglionic neurons secrete norepinephrine (NE), which targets adrenergic receptors on the target cells.

216
Q

Describe the neurotransmitter and receptor interaction for most parasympathetic postganglionic neurons.

A

Most parasympathetic postganglionic neurons release acetylcholine (ACh), which acts on muscarinic cholinergic receptors (mAChR) on the target cells.

217
Q

What are sympathetic cholinergic neurons, and where do they typically innervate?

A

Sympathetic cholinergic neurons are a unique subset of sympathetic postganglionic neurons that secrete acetylcholine (ACh) instead of norepinephrine. They typically innervate sweat glands.

218
Q

What are nonadrenergic, noncholinergic neurons, and what neurotransmitters do they use?

A

Nonadrenergic, noncholinergic neurons do not secrete norepinephrine or acetylcholine. They use alternative neurotransmitters such as substance P, somatostatin, vasoactive intestinal peptide (VIP), adenosine, nitric oxide, and ATP.

219
Q

How can some autonomic neurons co-secrete more than one neurotransmitter?

A

Some autonomic neurons have the ability to co-secrete multiple neurotransmitters, which allows for more complex and nuanced signaling to their target cells, enhancing the versatility of autonomic responses.

220
Q

What is a neuroeffector junction in the context of the autonomic nervous system?

A

The neuroeffector junction is the synapse between a postganglionic autonomic neuron and its target cell, also called an effector. This includes smooth muscle, cardiac muscle, glands, and other tissues controlled by the autonomic nervous system.

221
Q

How does the structure of an autonomic synapse differ from a typical synaptic junction?

A

Autonomic postganglionic axons end in varicosities, which are swollen areas containing neurotransmitter vesicles. Unlike typical synapses, these do not align with specific receptor sites on the target cell membrane but release neurotransmitters into the interstitial fluid, allowing for diffuse communication across a broad area of tissue.

222
Q

What are varicosities, and what role do they play in autonomic neurotransmission?

A

Varicosities are enlarged segments along the axon of a postganglionic neuron that store and release neurotransmitters. They facilitate a dispersed method of neurotransmission, enabling a single neuron to influence extensive areas of target tissue by diffusing neurotransmitters across a wide space.

223
Q

How is the release of neurotransmitters at neuroeffector junctions modulated?

A

The release of neurotransmitters at neuroeffector junctions can be modulated by various factors, including hormones and paracrine signals like histamine, which can either facilitate or inhibit neurotransmitter release from the varicosities.

224
Q

What is the significance of neuropeptides co-secreted with acetylcholine in autonomic pathways?

A

Neuropeptides co-secreted with acetylcholine by preganglionic neurons act as neuromodulators. They induce slow synaptic potentials that can prolong or modify the response of postganglionic neurons, affecting how effectively these neurons stimulate their target tissues.

225
Q

Describe how autonomic neurotransmission impacts the target tissues.

A

Autonomic neurotransmission impacts target tissues through a less localized, more diffuse release of neurotransmitters, allowing a broader modulation of tissue function compared to the direct and localized effects seen in somatic neurotransmission. This broad impact is crucial for coordinating widespread bodily responses necessary for maintaining homeostasis.

226
Q

How are acetylcholine and norepinephrine synthesized in the autonomic nervous system?

A

Both neurotransmitters are synthesized in the axon varicosities from small, readily available molecules using cytoplasmic enzymes. Acetylcholine is synthesized from acetyl CoA and choline, while norepinephrine is synthesized from the amino acid tyrosine.

227
Q

Describe the process of neurotransmitter release at autonomic varicosities.

A

When an action potential reaches a varicosity, voltage-gated calcium channels open, allowing Ca2+ to enter. This influx triggers the exocytosis of synaptic vesicles, releasing the neurotransmitter into the synaptic gap.

228
Q

What happens to neurotransmitters after they are released into the synapse?

A

After release, neurotransmitters can bind to receptors on the target cell, diffuse away from the synapse, get metabolized by extracellular enzymes, or be taken back up into the varicosities for reuse or degradation.

229
Q

How is norepinephrine recycled within autonomic varicosities?

A

Norepinephrine that is taken back into varicosities may be repackaged into vesicles for future release or metabolized by enzymes like monoamine oxidase (MAO) to terminate its action and maintain synaptic clarity.

230
Q

What factors influence the concentration of neurotransmitter in the synapse and its effect on the target cell?

A

The concentration of neurotransmitter in the synapse, crucial for determining the duration and strength of the response in the target cell, depends on the rate of neurotransmitter release, its breakdown, or its reuptake by surrounding cells and varicosities.

231
Q

Compare the roles of acetylcholine and norepinephrine in the autonomic nervous system.

A

Acetylcholine is primarily used by both sympathetic and parasympathetic preganglionic neurons and by parasympathetic postganglionic neurons, while norepinephrine is mainly released by sympathetic postganglionic neurons, each triggering specific receptors and responses depending on the target tissues.

232
Q

What are the main types of adrenergic receptors in the sympathetic nervous system, and how do they respond to catecholamines?

A

Adrenergic receptors are categorized into alpha (α) and beta (β) types, each with several subtypes. Alpha receptors generally respond more strongly to norepinephrine than epinephrine, while beta receptors vary in their response; β1 has equal affinity for both, β2 is more sensitive to epinephrine, and β3 is more sensitive to norepinephrine and primarily found in adipose tissue.

233
Q

How do beta adrenergic receptors differ in their physiological effects and distribution?

A

β1 receptors are typically found in the heart where they enhance contraction, β2 receptors are located in smooth muscle tissues like the lungs where they promote relaxation and are not directly innervated, and β3 receptors are mostly in adipose tissue affecting lipid metabolism.

234
Q

Describe the signaling mechanisms of adrenergic receptors

A

All adrenergic receptors are G protein-coupled receptors. Activation of β1 receptors triggers phospholipase C, producing IP3 and DAG, leading to protein phosphorylation and calcium signaling. α1 activation typically causes muscle contraction or secretion, while α2 decreases cAMP causing relaxation or decreased secretion. β receptors generally increase cAMP and promote phosphorylation of proteins.

235
Q

What types of neurotransmitters and receptors are characteristic of parasympathetic postganglionic neurons?

A

Parasympathetic postganglionic neurons primarily release acetylcholine (ACh), which acts on muscarinic cholinergic receptors (mAChR) on target tissues. These receptors are also G protein-coupled and influence cellular responses through various second messenger pathways.

236
Q

How do muscarinic receptors differ in their effects on target tissues?

A

Muscarinic receptors are classified into five subtypes (M1 to M5). Commonly, M2 receptors are found in the heart where they slow heart rate, and M3 receptors are located in smooth muscles and glands promoting contraction and secretion, respectively. Each subtype affects different ion channels or enzymes, leading to varied physiological responses.

237
Q

Explain the role of nonadrenergic, noncholinergic neurotransmitters in autonomic pathways.

A

Some autonomic neurons release other neurotransmitters such as substance P, VIP, and nitric oxide, which act through different receptors and mechanisms from classical neurotransmitters. These substances can modulate or mediate specific autonomic responses, particularly in non-traditional synaptic arrangements.

238
Q

What is the adrenal medulla and where is it located?

A

The adrenal medulla is the inner part of the adrenal glands, located atop the kidneys. It is a specialized neuroendocrine tissue that plays a key role in the sympathetic nervous system by secreting epinephrine.

239
Q

How does the adrenal medulla differ from the adrenal cortex?

A

The adrenal cortex is the outer layer of the adrenal glands and originates from epidermal tissue, secreting steroid hormones. In contrast, the adrenal medulla develops from neural tissue similar to sympathetic neurons and secretes catecholamines like epinephrine.

240
Q

Describe the embryological development of the adrenal medulla.

A

The adrenal medulla develops from the same embryonic tissue as sympathetic neurons. It forms the core of the adrenal glands and functions as a modified sympathetic ganglion.

241
Q

What is the role of chromaffin cells in the adrenal medulla?

A

Chromaffin cells in the adrenal medulla are axonless postganglionic neurons that secrete the neurohormone epinephrine directly into the bloodstream in response to sympathetic activation.

242
Q

How does the adrenal medulla contribute to the fight-or-flight response?

A

During a fight-or-flight response, the adrenal medulla releases large amounts of epinephrine into the blood under stimulation from preganglionic sympathetic neurons. This widespread distribution of epinephrine prepares various body systems to handle acute stress by enhancing alertness, increasing heart rate, and mobilizing energy

243
Q

Explain the neural connection to the adrenal medulla.

A

Preganglionic sympathetic neurons extend from the spinal cord directly to the adrenal medulla, where they synapse with chromaffin cells. Unlike typical postganglionic neurons, these cells release their secretions into the bloodstream rather than to specific target cells, amplifying the sympathetic response throughout the body.

244
Q

What are direct and indirect agonists and antagonists in the context of the autonomic nervous system?

A

Direct agonists and antagonists interact directly with autonomic receptors to mimic or block neurotransmitter effects. Indirect agonists and antagonists influence autonomic functions by altering neurotransmitter secretion, reuptake, or degradation.

245
Q

Give an example of an indirect agonist and explain its effects.

A

Cocaine is an indirect agonist that blocks the reuptake of norepinephrine, prolonging its excitatory effect, particularly on the heart, where prolonged sympathetic activity can lead to vasoconstriction and heart attacks.

246
Q

What are cholinesterase inhibitors, and what are their effects on the body?

A

Cholinesterase inhibitors prevent the degradation of acetylcholine, thereby extending its activity at synapses. Examples include toxic compounds like organophosphate insecticides and nerve gases, which cause symptoms due to excessive stimulation of autonomic and somatic motor target tissues.

247
Q

How do antidepressants act as indirect agonists?

A

Many antidepressants are indirect agonists that act by inhibiting neurotransmitter transporters (e.g., SSRIs for serotonin) or affecting their metabolism (e.g., MAO inhibitors for norepinephrine and serotonin), which can enhance mood-regulating neurotransmitter levels in the brain.

248
Q

Discuss the role of beta-blockers in treating high blood pressure.

A

Beta-blockers are drugs that specifically block beta adrenergic receptors, reducing heart rate and the force of heart contractions, thereby lowering blood pressure. They are a crucial tool in managing hypertension.

249
Q

What are common causes of autonomic nervous system dysfunction?

A

Autonomic nervous system dysfunction can be caused by direct trauma to hypothalamic control centers, systemic diseases like cancer and diabetes mellitus, and degenerative conditions such as multiple system atrophy that affect CNS control centers for autonomic functions.

250
Q

What is dysautonomia and its typical manifestations?

A

Dysautonomia refers to generalized dysfunction of the sympathetic nervous system, often resulting from systemic diseases. It commonly affects the cardiovascular system, leading to symptoms like abnormally low blood pressure due to reduced sympathetic input to blood vessels.

251
Q

Describe the impact of sympathetic dysfunction on urinary and sexual functions.

A

Sympathetic dysfunction can cause urinary incontinence, which is the loss of bladder control, and impotence, which is the inability to achieve or sustain an erection. These symptoms arise from diminished sympathetic nerve activity affecting normal muscular and vascular functions.

252
Q

What is primary autonomic failure and its consequences?

A

Primary autonomic failure occurs when sympathetic neurons degenerate, leading to chronic reduced sympathetic input. Affected tissues may respond by up-regulating their receptors (denervation hypersensitivity), making them overly responsive to any available neurotransmitters or similar drugs.

253
Q

What is denervation hypersensitivity and how does it affect the body?

A

Denervation hypersensitivity occurs when target tissues of diminished sympathetic input compensate by increasing receptor density. This leads to an exaggerated response to sympathetic neurotransmitters or exogenous adrenergic agonists, potentially causing severe physiological reactions.

254
Q

How does damage to hypothalamic control centers affect the body?

A

Damage to hypothalamic control centers can disrupt the body’s ability to regulate essential functions like water balance and temperature control, leading to significant homeostatic imbalances and systemic health issues.

255
Q

How are the neuronal pathways structured in both sympathetic and parasympathetic nervous systems?

A

Both systems typically consist of two neurons in series: a preganglionic neuron that originates in the CNS and a postganglionic neuron that reaches the target tissues. An exception is the adrenal medulla in the sympathetic system, where postganglionic neurons are modified into a neuroendocrine organ.

256
Q

What neurotransmitters are secreted by preganglionic and postganglionic neurons in the autonomic nervous system?

A

All preganglionic neurons, both sympathetic and parasympathetic, secrete acetylcholine onto nicotinic receptors. Most postganglionic sympathetic neurons secrete norepinephrine onto adrenergic receptors, while most parasympathetic postganglionic neurons secrete acetylcholine onto muscarinic receptors.

257
Q

Where do sympathetic and parasympathetic pathways originate within the CNS?

A

Sympathetic pathways originate in the thoracic and lumbar regions of the spinal cord, while parasympathetic pathways emanate from the brain stem and the sacral region of the spinal cord.

258
Q

What are the locations of the ganglia in sympathetic and parasympathetic systems?

A

Sympathetic ganglia are typically located close to the spinal cord (paravertebral), whereas parasympathetic ganglia are found close to or within the target tissues, facilitating rapid response to internal body changes.

259
Q

Describe the primary functions of the sympathetic and parasympathetic branches of the autonomic nervous system.

A

The sympathetic branch primarily prepares the body for stress and emergencies through the fight-or-flight response, enhancing alertness and metabolic output. Conversely, the parasympathetic branch supports rest-and-digest activities, promoting conservation and recovery of body energy.

260
Q

What is the structural composition of a somatic motor pathway?

A

Somatic motor pathways consist of a single neuron that originates in the CNS, with cell bodies typically located in the ventral horn of the spinal cord or in the brain. The neuron extends a long, myelinated axon directly to skeletal muscle fibers.

261
Q

How does the structure of a somatic motor neuron facilitate muscle control?

A

Somatic motor neurons have long axons that branch near their target skeletal muscles. Each branch ends in a cluster of enlarged axon terminals at the neuromuscular junction, allowing a single neuron to control multiple muscle fibers simultaneously.

262
Q

Describe the neuromuscular junction and its components

A

The neuromuscular junction (NMJ) is the synapse between a somatic motor neuron and a muscle fiber, consisting of the presynaptic axon terminal filled with synaptic vesicles, the synaptic cleft, and the postsynaptic motor end plate on the muscle fiber. Schwann cells cover the axon terminals, contributing to NMJ maintenance and formation.

263
Q

What role do Schwann cells play at the neuromuscular junction?

A

Schwann cells form a thin layer over the axon terminals at the NMJ, secreting chemical signal molecules that are crucial for the development and maintenance of the junction, providing more than just insulation for electrical impulses.

264
Q

What is unique about the motor end plate at the NMJ?

A

The motor end plate is a specialized part of the muscle cell membrane with deep folds (like shallow gutters) that increase the surface area for synaptic contact. It houses densely clustered nicotinic ACh receptors in the active zones, enhancing neuromuscular transmission.

265
Q

How is acetylcholine (ACh) managed at the neuromuscular junction?

A

ACh released into the synaptic cleft binds to receptors on the motor end plate to initiate muscle contraction. It is rapidly degraded by acetylcholinesterase (AChE), an enzyme in the synaptic cleft, into acetyl and choline, terminating the signal and preventing continuous muscle contraction.

266
Q

How do action potentials trigger neurotransmitter release at the neuromuscular junction?

A

Action potentials arriving at the axon terminal open voltage-gated calcium channels, allowing Ca2+ to enter. This influx triggers the exocytosis of ACh-containing synaptic vesicles, releasing acetylcholine into the synaptic cleft.

267
Q

What is the function of nAChRs on skeletal muscle membranes, and how do they differ from those on neurons?

A

nAChRs on skeletal muscles (NM subtype) consist of α, β, δ, and ε subunits and open to allow Na+ influx, depolarizing the muscle and triggering contraction. This contrasts with neuronal nAChRs (NN subtype), which have only α and β subunits and are not sensitive to α-bungarotoxin like muscle receptors

268
Q

How does acetylcholine act on skeletal muscle fibers?

A

ACh binds to nicotinic receptors on the muscle’s motor end plate, opening ion channels that allow Na+ to enter the muscle fiber. This causes depolarization and an action potential, leading to muscle contraction.

269
Q

What mechanisms lead to muscle relaxation in the somatic motor system?

A

Muscle relaxation occurs not by any direct antagonistic action at the neuromuscular junction but by inhibiting the release of ACh from somatic motor neurons in the CNS. This prevents further muscle contraction signals from being sent.

270
Q

Discuss the importance of somatic motor neurons for muscle health.

A

Somatic motor neurons are crucial not only for initiating muscle contractions but also for maintaining muscle health. Regular use of muscles maintains their mass and function; without synaptic input from motor neurons, muscles weaken and deteriorate, impacting movement, posture, and even breathing.

271
Q

What is myasthenia gravis and how does it affect neuromuscular function?

A

Myasthenia gravis is an autoimmune disorder characterized by the loss of ACh receptors at the neuromuscular junction. This leads to weakened muscle contractions, fatigue, and potentially severe impairment of respiratory function, requiring interventions like artificial ventilation in extreme cases.

272
Q
A