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Y1 Fundamentals of Neuroscience and Pharmacology > L9: The Neuromuscular Junction > Flashcards

L9: The Neuromuscular Junction Flashcards

1
Q

What is the neuromuscular junction?

A

It is a specialized synapse between a motor neuron and a skeletal muscle fiber, ensuring reliable and rapid signal transmission.

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2
Q

What neurotransmitter is primarily involved in the neuromuscular junction?

A

Acetylcholine (ACh).

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3
Q

What structure increases the surface area of the postsynaptic membrane at the neuromuscular junction?

A

Junctional folds.

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4
Q

What enzyme terminates the signal at the neuromuscular junction?

A

Acetylcholinesterase.

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5
Q

What are the main ion movements during postsynaptic depolarization in the neuromuscular junction?

A

Sodium ions (Na⁺) enter the cell, and potassium ions (K⁺) leave.

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6
Q

What receptor type is found on the postsynaptic membrane of the neuromuscular junction?

A

Nicotinic acetylcholine receptors.

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7
Q

How is the action potential initiated at the neuromuscular junction propagated into the muscle fiber?

A

Through the T-tubule system.

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8
Q

What is the main role of the sarcoplasmic reticulum in muscle contraction?

A

To store and release calcium ions (Ca²⁺), which trigger muscle contraction.

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9
Q

What condition is characterized by fatigue and muscle weakness due to neuromuscular junction dysfunction?

A

Myasthenia Gravis.

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10
Q

How does Myasthenia Gravis impair neuromuscular transmission?

A

It involves antibodies attacking nicotinic acetylcholine receptors, reducing their number and function.

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11
Q

What type of drug is used to treat Myasthenia Gravis?

A

Acetylcholinesterase inhibitors, which prolong the presence of acetylcholine in the synaptic cleft.

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12
Q

What is an end-plate potential?

A

A large depolarization at the neuromuscular junction caused by acetylcholine receptor activation.

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13
Q

What ion is critical for neurotransmitter release at the presynaptic terminal?

A

Calcium ions (Ca²⁺).

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14
Q

What are the two electrical events at the neuromuscular junction?

A

The ligand-gated sodium influx causing depolarization, followed by action potential propagation via voltage-gated sodium channels.

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15
Q

How is calcium involved in presynaptic neurotransmitter release?

A

Voltage-gated calcium channels open, allowing calcium to enter and trigger vesicle fusion with the membrane.

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16
Q

What is the main function of the neuromuscular junction?

A

To reliably transmit signals from motor neurons to muscle fibers, resulting in muscle contraction.

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17
Q

Where are the cell bodies of motor neurons located?

A

In the ventral horn of the spinal cord.

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18
Q

What distinguishes the neuromuscular junction from synapses in the central nervous system?

A

It is highly specialized, with structural features like junctional folds and high densities of acetylcholine receptors to ensure reliable signal transmission.

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19
Q

What is the role of voltage-gated calcium channels in the presynaptic terminal?

A

They open in response to depolarization, allowing calcium ions to enter and trigger vesicle exocytosis.

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20
Q

What is the calcium sensor protein that initiates vesicle fusion during exocytosis?

A

Synaptotagmin.

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21
Q

How does acetylcholine cause depolarization in the postsynaptic muscle cell?

A

By binding to nicotinic receptors, opening ion channels that allow sodium influx and potassium efflux.

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22
Q

What is the effect of the large depolarization caused by acetylcholine at the neuromuscular junction?

A

It triggers an action potential that propagates across the muscle membrane.

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23
Q

What is the function of the T-tubule system in muscle fibers?

A

It transmits the action potential deep into the muscle to activate contraction mechanisms.

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24
Q

What is the DHP receptor, and what is its role in muscle contraction?

A

The DHP receptor (dihydropyridine receptor) is a voltage sensor that triggers calcium release from the sarcoplasmic reticulum.

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25
Q

What channel releases calcium from the sarcoplasmic reticulum into the muscle cytoplasm?

A

The ryanodine receptor.

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26
Q

Why is rapid acetylcholine breakdown important at the neuromuscular junction?

A

To ensure precise control of muscle contraction and prevent continuous stimulation.

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27
Q

How does myasthenia gravis affect eye muscles specifically?

A

Eye muscles are used frequently, making them more prone to fatigue in this condition.

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28
Q

What is temporal summation in the context of muscle contraction?

A

The increase in muscle contraction strength when stimuli are delivered in rapid succession.

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29
Q

How does the neuromuscular junction achieve reliable transmission?

A

Through high densities of acetylcholine receptors, abundant synaptic vesicles, and structural adaptations like junctional folds.

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30
Q

What happens if acetylcholinesterase is inhibited?

A

Acetylcholine remains in the synaptic cleft longer, enhancing receptor activation and muscle contraction.

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31
Q

What is the resting membrane potential of the neuromuscular junction, and how does it compare to central nervous system synapses?

A

It is approximately -90 mV, which is more negative than the typical -65 mV in central nervous system neurons.

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32
Q

What is the role of ligand-gated ion channels in the neuromuscular junction?

A

They mediate the initial depolarization by allowing sodium influx upon acetylcholine binding.

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33
Q

What is the significance of multiple vesicle release in the neuromuscular junction?

A

It ensures a large release of acetylcholine, resulting in a strong and reliable depolarization (end-plate potential).

34
Q

What clinical symptom is most commonly associated with myasthenia gravis?

A

Muscle weakness, particularly in the eyes and eyelids, due to rapid fatigue of affected muscles.

35
Q

What distinguishes the postsynaptic membrane at the neuromuscular junction?

A

It has junctional folds that increase the surface area for acetylcholine receptor expression, enhancing signal transmission efficiency.

36
Q

What causes the release of neurotransmitters in the presynaptic terminal?

A

An influx of calcium ions (Ca²⁺) into the presynaptic terminal triggers vesicle fusion and neurotransmitter release.

37
Q

What happens during exocytosis at the neuromuscular junction?

A

Vesicles containing acetylcholine fuse with the presynaptic membrane, releasing the neurotransmitter into the synaptic cleft.

38
Q

What is the role of the sarcoplasmic reticulum in muscle contraction?

A

It stores calcium ions and releases them in response to signals, initiating muscle contraction.

39
Q

What ensures that acetylcholine release reliably triggers muscle contraction?

A

The large number of acetylcholine-containing vesicles and the high density of postsynaptic receptors.

40
Q

How is acetylcholine synthesized in the neuron?

A

From choline and acetyl-CoA, catalyzed by the enzyme choline acetyltransferase.

41
Q

What is the fate of acetylcholine after it has bound to receptors?

A

It is broken down into acetate and choline by acetylcholinesterase, and choline is taken back up by the presynaptic neuron for reuse.

42
Q

What is the difference between ligand-gated and voltage-gated ion channels at the neuromuscular junction?

A

Ligand-gated channels open in response to acetylcholine binding, while voltage-gated channels open in response to changes in membrane potential.

43
Q

What is the equilibrium potential for sodium (Na⁺) at the neuromuscular junction?

A

Approximately +60 mV, which drives sodium into the cell during depolarization.

44
Q

What is the equilibrium potential for potassium (K⁺) at the neuromuscular junction?

A

Approximately -90 mV, which means potassium has little initial driving force but increases as depolarization progresses.

45
Q

Why does potassium eventually flow out of the cell during depolarization?

A

Depolarization moves the membrane potential away from potassium’s equilibrium potential, creating a driving force for its efflux.

46
Q

What are the two main phases of electrical signaling at the neuromuscular junction?

A

The initial ligand-gated depolarization and the subsequent action potential propagation via voltage-gated sodium channels.

47
Q

What is summation in the context of muscle contraction?

A

The additive effect of multiple rapid signals leading to sustained contraction rather than individual twitches.

48
Q

What structural feature allows the action potential to invade the interior of the muscle fiber?

A

The T-tubule system (transverse tubules).

49
Q

How does depolarization lead to calcium release from the sarcoplasmic reticulum?

A

The DHP receptor detects depolarization and triggers the ryanodine receptor to release calcium from the sarcoplasmic reticulum.

50
Q

What condition results from the immune system attacking acetylcholine receptors at the neuromuscular junction?

A

Myasthenia Gravis.

51
Q

Why is calcium critical for both neurotransmitter release and muscle contraction?

A

It triggers vesicle fusion for neurotransmitter release and activates contractile proteins in the muscle.

52
Q

What is the typical duration of a synaptic event at the neuromuscular junction?

A

Approximately 1 millisecond.

53
Q

What electrical event propagates along the muscle membrane after the initial depolarization?

A

An action potential.

54
Q

How is the large depolarization at the neuromuscular junction termed?

A

End-plate potential (EPP).

55
Q

What happens to calcium after muscle contraction is completed?

A

It is pumped back into the sarcoplasmic reticulum to terminate contraction and reset the system.

56
Q

What is the main structural difference between the neuromuscular junction and central nervous system synapses?

A

The neuromuscular junction has junctional folds and a much higher density of acetylcholine receptors, while CNS synapses have fewer receptors and lack such folds.

57
Q

How does acetylcholine binding affect nicotinic acetylcholine receptors?

A

It causes a conformational change that opens an ion channel, allowing sodium (Na⁺) to enter and potassium (K⁺) to exit the muscle cell.

58
Q

What ensures the rapid onset of action potentials at the neuromuscular junction?

A

The high density of voltage-gated sodium channels near the end-plate potential ensures efficient propagation of the signal.

59
Q

What are the primary forces driving sodium (Na⁺) influx during depolarization?

A

Sodium influx is driven by both a chemical gradient (higher Na⁺ concentration outside the cell) and an electrical gradient (negative resting membrane potential).

60
Q

Why is there minimal potassium (K⁺) efflux at the start of depolarization?

A

The resting membrane potential is close to potassium’s equilibrium potential, resulting in a weak driving force for potassium efflux initially.

61
Q

What happens to the postsynaptic membrane potential during an end-plate potential (EPP)?

A

The membrane potential depolarizes from approximately -90 mV towards the threshold for an action potential.

62
Q

What proteins are involved in vesicle docking and fusion during neurotransmitter release?

A

SNARE proteins and synaptotagmin play key roles in the docking and fusion of vesicles with the presynaptic membrane.

63
Q

What role does the DHP receptor play in excitation-contraction coupling?

A

It acts as a voltage sensor that triggers the ryanodine receptor to release calcium from the sarcoplasmic reticulum.

64
Q

What is the function of the ryanodine receptor in muscle contraction?

A

It releases calcium ions from the sarcoplasmic reticulum in response to signals from the DHP receptor, initiating contraction.

65
Q

How is acetylcholine synthesized and stored?

A

Acetylcholine is synthesized from choline and acetyl-CoA by choline acetyltransferase and stored in vesicles in the presynaptic terminal.

66
Q

What is a quantum of neurotransmitter release?

A

A quantum refers to the release of acetylcholine from a single vesicle, typically containing around 4,000 molecules of acetylcholine.

67
Q

Why is the neuromuscular junction considered highly reliable for signal transmission?

A

It has a high density of acetylcholine receptors, abundant vesicles, and structural features like junctional folds that ensure effective neurotransmitter binding and signal propagation.

68
Q

What are the clinical manifestations of myasthenia gravis?

A

Symptoms include muscle weakness, especially in the eyes and eyelids, difficulty swallowing, and fatigue with sustained activity.

69
Q

How does an acetylcholinesterase inhibitor work to treat myasthenia gravis?

A

It prevents the breakdown of acetylcholine in the synaptic cleft, prolonging its action and improving muscle contraction.

70
Q

What electrical events differentiate ligand-gated and voltage-gated ion channels in the neuromuscular junction?

A

Ligand-gated channels respond to acetylcholine and initiate depolarization, while voltage-gated channels propagate the action potential along the muscle membrane.

71
Q

How does the neuromuscular junction amplify the signal for muscle contraction?

A

By releasing large quantities of acetylcholine and activating numerous receptors, leading to a strong depolarization (end-plate potential) and a robust action potential.

72
Q

What is temporal summation in the context of muscle twitches?

A

It is the additive effect of multiple action potentials arriving in rapid succession, increasing muscle contraction strength.

73
Q

What is spatial summation, and how does it differ from temporal summation?

A

Spatial summation refers to multiple inputs converging on a single neuron, common in the CNS, while temporal summation involves the frequency of action potentials increasing contraction in a muscle fiber.

74
Q

Why does the neuromuscular junction have such a high density of acetylcholine receptors?

A

To ensure that the large amount of acetylcholine released can reliably trigger a strong and rapid depolarization.

75
Q

How does calcium signaling differ presynaptically and postsynaptically in the neuromuscular junction?

A

Presynaptically, calcium influx triggers vesicle fusion and neurotransmitter release. Postsynaptically, calcium released from the sarcoplasmic reticulum activates contraction.

76
Q

What happens to the sarcoplasmic reticulum after muscle contraction is completed?

A

Calcium is pumped back into the sarcoplasmic reticulum by calcium pumps, terminating the contraction and resetting the system.

77
Q

What is the typical time course of a synaptic event at the neuromuscular junction?

A

The neurotransmitter release and postsynaptic depolarization last about 1 millisecond.

78
Q

How does the neuromuscular junction prevent overstimulation of muscle fibers?

A

Acetylcholine is rapidly broken down by acetylcholinesterase, terminating the signal.

79
Q

What is the purpose of the T-tubule system in muscle fibers?

A

It ensures the action potential reaches deep into the muscle fiber.

80
Q

What is the purpose of the T-tubule system in muscle fibers?

A

It ensures the action potential spreads deep into the muscle, activating contraction mechanisms throughout the fiber.

81
Q

What structural feature of the neuromuscular junction facilitates high-frequency synaptic transmission?

A

Its large surface area, high receptor density, and extensive junctional folds optimize neurotransmitter binding and signal propagation.

Y1 Fundamentals of Neuroscience and Pharmacology (11 decks)

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