Capitolo 7 Flashcards

(25 cards)

1
Q

What is the role of Schwann cells at the neuromuscular junction (NMJ)?

A

Schwann cells provide insulation and protection to the branching nerve terminals at the neuromuscular junction.

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2
Q

What is the purpose of subneural clefts in the NMJ?

A

Subneural clefts increase the surface area for neurotransmitter interaction, enhancing the efficiency of signal transmission.

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3
Q

How is acetylcholine synthesized and stored in the nerve terminal?

A

Acetylcholine is synthesized in the cytoplasm of the nerve terminal and stored in approximately 300,000 synaptic vesicles.

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4
Q

What triggers the release of acetylcholine from the nerve terminal?

A

The release of acetylcholine is triggered by an action potential, which opens voltage-gated calcium channels, allowing calcium ions to enter the nerve terminal.

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5
Q

What happens when acetylcholine binds to receptors on the muscle fiber membrane?

A

Acetylcholine binding causes depolarization of the muscle fiber membrane, triggering an action potential that leads to muscle contraction.

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6
Q

What is the role of acetylcholine in opening the ion channel?

A

Acetylcholine binds to the two alpha subunits of the receptor, causing a conformational change that opens the ion channel.

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7
Q

What ions can pass through the acetylcholine receptor ion channel, and which are repelled?

A

Sodium (Na⁺), potassium (K⁺), and calcium (Ca²⁺) ions can pass through, while negatively charged ions like chloride (Cl⁻) are repelled.

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8
Q

Why is sodium influx greater than potassium efflux in the acetylcholine receptor channel?

A

Sodium influx is greater due to the high extracellular sodium concentration and the negative resting membrane potential, which attracts sodium into the fiber and prevents significant potassium efflux.

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9
Q

What is the end plate potential (EPP), and how does it contribute to muscle contraction?

A

The EPP is a local positive potential generated by sodium influx through the acetylcholine receptor. It depolarizes the membrane enough to open voltage-gated sodium channels, initiating an action potential that spreads and triggers muscle contraction.

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10
Q

What is the difference between fetal and adult acetylcholine receptors?

A

In fetal receptors, the subunit composition includes gamma, while in adult receptors, the gamma subunit is replaced by epsilon.

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11
Q

What is the function of acetylcholinesterase at the neuromuscular junction?

A

Acetylcholinesterase rapidly degrades acetylcholine in the synaptic space, preventing prolonged receptor activation and allowing muscle fibers to recover quickly.

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12
Q

What is the threshold of the end plate potential (EPP) needed to initiate an action potential?

A

The EPP must exceed a threshold of 20 to 30 millivolts to trigger an action potential.

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13
Q

How do curare and botulinum toxin affect neuromuscular transmission?

A

Curare competes with acetylcholine for receptor binding, weakening the EPP and reducing muscle activation. Botulinum toxin reduces acetylcholine release, impairing EPP generation and neuromuscular transmission.

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14
Q

What is the neuromuscular junction’s safety factor, and why is it important?

A

The safety factor ensures that the EPP is about three times stronger than the minimum required to stimulate muscle fibers, ensuring reliable muscle contraction under normal conditions.

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15
Q

What causes neuromuscular junction fatigue, and how does it affect transmission?

A

Fatigue occurs during high-frequency stimulation (over 100 times per second), depleting acetylcholine vesicles and increasing the risk of transmission failure.

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16
Q

What is the resting membrane potential of skeletal muscle fibers, and how does it compare to neurons?

A

The resting membrane potential of skeletal muscle fibers is approximately −80 to −90 millivolts, which is 10 to 20 millivolts more negative than that of neurons.

17
Q

How does the duration of the action potential in skeletal muscle compare to that in large myelinated nerve fibers?

A

The action potential in skeletal muscle lasts 1 to 5 milliseconds, about five times longer than in large myelinated nerve fibers.

18
Q

Why do skeletal muscle fibers require transverse tubules (T tubules)?

A

Skeletal muscle fibers are large, so T tubules are necessary to transmit action potentials deep into the muscle, near the myofibrils, ensuring efficient calcium release and muscle contraction.

19
Q

What is the velocity of conduction in skeletal muscle fibers, and how does it compare to that in large myelinated nerve fibers?

A

The conduction velocity in skeletal muscle fibers is 3 to 5 m/s, about 1/13 of the velocity in large myelinated nerve fibers.

20
Q

What process links the action potential to muscle contraction?

A

The process is called excitation-contraction coupling, where the action potential traveling through T tubules triggers calcium ion release, leading to muscle contraction.

21
Q

What is the role of the transverse tubules (T tubules) in excitation-contraction coupling?

A

The T tubules transmit action potentials deep into the muscle fiber, allowing communication with the sarcoplasmic reticulum (SR) and initiating calcium ion release for muscle contraction.

22
Q

How do dihydropyridine and ryanodine receptors work together during muscle contraction?

A

Dihydropyridine receptors on the T tubules detect the voltage change from the action potential and activate ryanodine receptors in the SR, causing calcium release into the sarcoplasm.

23
Q

What is the function of the SERCA pump in muscle relaxation?

A

The SERCA pump actively transports calcium ions back into the sarcoplasmic reticulum, reducing cytosolic calcium levels and terminating muscle contraction.

24
Q

How does calsequestrin assist in calcium storage within the sarcoplasmic reticulum?

A

Calsequestrin binds up to 40 calcium ions per molecule, helping to store high concentrations of calcium ions in the sarcoplasmic reticulum efficiently.

25
What is the difference in the duration of the calcium pulse between skeletal and cardiac muscle?
In skeletal muscle, the calcium pulse lasts about 1/20 of a second, while in cardiac muscle it lasts longer, about one-third of a second.