Neurology Chapter 5: Synaptic Transmission

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Questions and Answers

What is the first event that occurs during excitation-contraction coupling?

Release of Ca2+ from the sarcoplasmic reticulum

Development of an end-plate potential at the motor end plate (correct)

Binding of myosin to actin in the myofilaments

Initiation and propagation of an action potential along the sarcolemma

Which structure is involved in the propagation of action potential during muscle contraction?

Myofilaments

Sarcoplasmic reticulum

Z-discs

T-tubules (correct)

During which process is Ca2+ released, leading to muscle contraction?

Contraction cycle

Resting membrane potential

Excitation-contraction coupling (correct)

Muscle relaxation phase

What is the relationship between the T-tubules and terminal cisternae during muscle contraction?

They are connected directly without space Signup and view all the answers

Which of the following correctly describes a role of the sarcolemma in muscle contraction?

Transmits the action potential throughout the muscle fiber Signup and view all the answers

What role does calcium play in the release of acetylcholine at the synaptic knob?

Calcium triggers the fusion of synaptic vesicles with the plasma membrane. Signup and view all the answers

What occurs immediately after the binding of acetylcholine at the motor end plate?

The skeletal muscle fiber experiences excitation. Signup and view all the answers

Which alteration in the process of nerve signal propagation would most likely affect the calcium entry in the synaptic knob?

Blocking the function of voltage-gated Ca2+ channels. Signup and view all the answers

What might happen if acetylcholinesterase is inhibited in the synaptic cleft?

ACh would accumulate in the synaptic cleft, leading to prolonged muscle contraction. Signup and view all the answers

What is the effect of repeated nerve signals on the synaptic knob?

It enhances calcium influx into the synaptic knob. Signup and view all the answers

What happens to the resting membrane potential when an end-plate potential is established?

It changes to -65 mV. Signup and view all the answers

During which phase of the action potential does the inside of the sarcolemma become positive?

Depolarization Signup and view all the answers

What triggers the opening of voltage-gated channels in the sarcolemma?

A sufficient end-plate potential (EPP) Signup and view all the answers

What is the primary ion responsible for the rapid depolarization of the sarcolemma?

Na+ Signup and view all the answers

What occurs immediately after the initial influx of Na+ during the action potential?

K+ begins to diffuse out of the fiber. Signup and view all the answers

Which of the following statements describes the nature of the end-plate potential (EPP)?

It is both transient and local. Signup and view all the answers

What is the initial consequence of calcium binding to troponin?

Troponin undergoes a conformational change. Signup and view all the answers

During the power stroke, which of the following events occurs?

ADP and inorganic phosphate ($P_i$) are released. Signup and view all the answers

What is required for the release of the myosin head from actin?

ATP binding to the myosin head. Signup and view all the answers

What does the term 'cocked' position refer to in muscle contraction?

Myosin heads are in a position ready to form crossbridges. Signup and view all the answers

How does the troponin-tropomyosin complex affect muscle contraction?

It regulates the availability of myosin-binding sites on actin. Signup and view all the answers

What initiates the depolarization process in a skeletal muscle fiber?

The opening of voltage-gated Na+ channels Signup and view all the answers

What is the membrane potential at which depolarization occurs?

+30 mV Signup and view all the answers

What is the role of voltage-gated K+ channels during and after depolarization?

To restore the membrane potential to its resting state Signup and view all the answers

How does depolarization propagate along the sarcolemma and T-tubules?

By the sequential opening of voltage-gated Na+ channels Signup and view all the answers

What happens immediately after the opening of voltage-gated Na+ channels?

The voltage-gated K+ channels open Signup and view all the answers

Which ion movement primarily drives the depolarization of the skeletal muscle fiber?

Sodium ions entering the fiber Signup and view all the answers

What effect does the influx of Na+ ions have on membrane potential?

It reverses the membrane potential to a positive value Signup and view all the answers

What is the first step following the restoration of the membrane potential in a skeletal muscle fiber?

Repolarization of the membrane occurs Signup and view all the answers

What is the primary role of K+ ions during repolarization of skeletal muscle fibers?

K+ ions exit the cell to restore the negative membrane potential. Signup and view all the answers

What occurs after the depolarization phase of an action potential in skeletal muscle?

A brief refractory period follows. Signup and view all the answers

Which of the following correctly describes the sequence of events in an action potential within skeletal muscle?

Depolarization is followed by repolarization, both facilitated by voltage-gated channels. Signup and view all the answers

How does the refractory period influence the muscle's ability to respond to stimuli?

It prevents any new action potentials from occurring. Signup and view all the answers

What is the resting membrane potential (RMP) in skeletal muscle fibers?

-90 mV Signup and view all the answers

Why is repolarization crucial for skeletal muscle function?

It reestablishes the resting membrane potential for future action potentials. Signup and view all the answers

What mechanism parallels action potential propagation in both skeletal muscle and neurons?

The sequential opening of voltage-gated ion channels. Signup and view all the answers

Which of the following statements about the refractory period is true?

It is a phase during which a muscle cannot be restimulated. Signup and view all the answers

During the repolarization phase, what is the membrane potential typically moving towards?

$-90$ mV Signup and view all the answers

What initiates the changes in membrane voltage associated with an action potential at the sarcolemma?

The opening of Na+ channels Signup and view all the answers

What is the purpose of the conformational change in dihydropyridine receptors during excitation-contraction coupling?

To trigger Ca2+ release from the sarcoplasmic reticulum Signup and view all the answers

Which event occurs after the action potential reaches the triad?

Release of Ca2+ from the terminal cisternae Signup and view all the answers

What ion diffuses into the cytosol after the action potential stimulates the T-tubules?

Ca2+ Signup and view all the answers

Which of the following statements about the action potential is FALSE?

It takes several seconds to complete. Signup and view all the answers

What is the primary function of the voltage-gated K+ channels in the action potential process?

To repolarize the membrane Signup and view all the answers

Where does the Ca2+ released from the sarcoplasmic reticulum interact within myofibrils?

With both thick and thin filaments Signup and view all the answers

What is the role of the ryanodine receptors in excitation-contraction coupling?

To release Ca2+ into the cytosol Signup and view all the answers

What triggers the conformational change in the ryanodine receptors?

Conformational change in dihydropyridine receptors Signup and view all the answers

What happens immediately after calcium ions diffuse into the cytosol?

They bind to thick and thin filaments to promote contraction Signup and view all the answers

Study Notes

Calcium Entry at Synaptic Knob

Nerve signals trigger voltage-gated Ca2+ channels to open, allowing Ca2+ to flow down its concentration gradient into the synaptic knob.
Ca2+ binds to synaptotagmin on synaptic vesicles, triggering their fusion with the knob plasma membrane.

Release of ACh from Synaptic Knob

Fusion of synaptic vesicles with the knob membrane results in exocytosis of acetylcholine (ACh) into the synaptic cleft.
Approximately 300 vesicles release thousands of ACh molecules per nerve signal.

Binding of ACh at Motor End Plate

ACh diffuses across the synaptic cleft and binds to ACh receptors on the motor end plate.
This binding excites the skeletal muscle fiber.

Skeletal Muscle Fiber: Excitation-Contraction Coupling

Links the events of skeletal muscle stimulation to the events of contraction.
Involves the sarcolemma, T-tubules, and sarcoplasmic reticulum.
Three events occur during excitation-contraction coupling:
- Development of an end-plate potential at the motor end plate.
- Initiation and propagation of an action potential along the sarcolemma and T-tubules.
- Release of Ca2+ from the sarcoplasmic reticulum.

Development of an End-Plate Potential at the Motor End Plate

ACh binding to receptors opens chemically gated ion channels.
Na+ rapidly diffuses into the muscle fiber, and K+ slowly diffuses out.
More Na+ influx than K+ efflux results in a net positive charge inside the fiber.
This creates a local and transient end-plate potential (EPP).
If the EPP reaches a threshold of -65 mV, it triggers the opening of voltage-gated channels in the sarcolemma.

Initiation and Propagation of Action Potential Along the Sarcolemma and T-Tubules

The EPP triggers an action potential that propagates along the sarcolemma and T-tubules.
Action potential involves two events:
- Depolarization: The inside of the sarcolemma becomes positive due to Na+ influx.
- Repolarization: The inside of the sarcolemma returns to its negative resting potential due to K+ efflux.

Muscle Fiber Depolarization

The opening of voltage-gated Na+ channels in the motor end plate stimulates adjacent areas of the sarcolemma.
Na+ rapidly moves across the sarcolemma into the muscle fiber.
Sufficient Na+ influx reverses the membrane potential from negative to positive (+30 mV).
This reversal is called depolarization.
Depolarization ends when voltage-gated Na+ channels close.
Depolarization propagates along the sarcolemma and T-tubules due to sequential opening of voltage-gated Na+ channels.

Action Potentials in Skeletal Muscle

Repolarization: K+ efflux restores the negative resting membrane potential (-90 mV).
The opening of voltage-gated K+ channels occurs sequentially after depolarization, propagating repolarization.
Action potential is a self-sustaining, propagated electrical change in the membrane potential caused by sequential opening of voltage-gated channels.
The refractory period is a brief time during which the muscle cannot be restimulated.

Release of Calcium from the Sarcoplasmic Reticulum

When the action potential reaches a triad, it stimulates a conformational change in voltage-sensitive Ca2+ channels (dihydropyridine receptors) in the T-tubule membrane.
This change causes a conformational change in Ca2+ release channels (ryanodine receptors) in the terminal cisternae of the sarcoplasmic reticulum, triggering their opening.
Ca2+ diffuses from the terminal cisternae into the cytosol, mingling with the thick and thin filaments within myofibrils.

Calcium Binding

Ca2+ released from the sarcoplasmic reticulum binds to troponin, a component of thin filaments.
This causes a conformational change in troponin, moving the troponin-tropomyosin complex and exposing myosin binding sites on actin.
Crossbridge cycling begins.

Crossbridge Cycling

Crossbridge cycling is a four-step process:
- Crossbridge formation: Myosin heads attach to exposed myosin-binding sites on actin. This forms a crossbridge between the thick and thin filaments.
- Power stroke: The myosin head swivels, pulling the thin filament a short distance towards the sarcomere center. ADP and Pi are released.
- Release of myosin head: ATP binds to the myosin head, causing its release from actin.
- Resetting the myosin head: ATP is split into ADP and Pi, providing energy to reset the myosin head.

Sarcomere Function

The sarcomere is the basic contractile unit of a muscle fiber.
The contraction cycle involves multiple steps:
- Myosin head release: ATP binding causes the myosin head to detach from the actin binding site.
- Resetting the myosin head: ATP is split into ADP and Pi, resetting the myosin head.
- Attachment: The myosin head attaches to the actin binding site.
- Power stroke: The myosin head pulls on the actin filament.
- Release: ADP is released, causing the myosin head to detach.
- Reset: The myosin head returns to its original position.
These steps repeat as long as Ca2+ levels remain elevated.

Sarcomere Shortening

During contraction, the H zone disappears, the I band narrows or disappears, and the Z discs move closer together.
The thin and thick filaments themselves do not shorten; this is called the sliding filament theory.

Muscular Paralysis and Neurotoxins

Muscular paralysis can occur if nervous system function at the neuromuscular junction or excitation-contraction coupling is damaged.
Neurotoxins can damage nervous system components, leading to paralysis.
Two examples of paralysis caused by toxins are tetanus and botulism.

Tetanus

Caused by a toxin produced by Clostridium tetani.
The toxin blocks glycine release, leading to overstimulation of muscles by motor neurons and excessive contractions.

Botulism

Caused by a toxin produced by Clostridium botulinum.
The toxin prevents ACh release at synaptic knobs, leading to muscular paralysis.
Often results from ingesting the toxin in improperly processed canned foods.

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Description

This quiz focuses on the mechanisms of synaptic transmission, specifically the roles of calcium in synaptic knobs and the release of acetylcholine (ACh). It covers the binding of ACh at the motor end plate and the excitation-contraction coupling in skeletal muscle fibers. Test your understanding of these crucial neurological processes.