Neuromuscular Junction Sequence and Disorders

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Questions and Answers

What occurs when acetylcholine binds to its receptor sites?

It prevents Na+ and K+ from entering the motor end plate.
It closes the ligand-gated Na+ channel.
It decreases the permeability of the motor end plate to Na+ and K+.
It causes conformational changes that open the ligand-gated Na+ channel. (correct)

What is the role of ligand-gated Na+ channels at the motor end plate?

They prevent muscle contraction by blocking ion flow.
They increase permeability to both Na+ and K+ when opened. (correct)
They regulate muscle temperature.
They exclusively permit K+ ions to flow through.

Which ion's influx is primarily facilitated by the opening of ligand-gated Na+ channels?

Sodium ions (Na+) (correct)
Potassium ions (K+)
Calcium ions (Ca2+)
Chloride ions (Cl-)

What is the role of acetylcholine in the neuromuscular junction?

It acts as a signaling molecule that travels across the synaptic cleft. (D) Signup and view all the answers

What initiates the conformational changes necessary for opening ligand-gated Na+ channels?

The binding of acetylcholine to its receptor sites. (C) Signup and view all the answers

What is the consequence of the conformational changes in ligand-gated Na+ channels?

Increased permeability to multiple ions. (D) Signup and view all the answers

Where is acetylcholine stored before it is released into the synaptic cleft?

In synaptic vesicles located in the presynaptic terminal (B) Signup and view all the answers

What happens to acetylcholine after it diffuses across the synaptic cleft?

It binds to receptors on the postsynaptic membrane. (A) Signup and view all the answers

Which ion is primarily involved in the release of acetylcholine from the presynaptic terminal?

Ca2+ (Calcium) (A) Signup and view all the answers

What is the significance of the synaptic cleft in neuromuscular transmission?

It allows for the transmission of signals between neurons and muscle cells. (B) Signup and view all the answers

Study Notes

Neuromuscular Junction (NMJ) Sequence of Events (Continued)

Calcium ions (Ca2+) enter the presynaptic terminal, triggering the release of acetylcholine (Ach) from synaptic vesicles.
Ach diffuses across the synaptic cleft to the postsynaptic membrane, also known as the motor end plate.
Ach binds to its receptor sites on the motor end plate, causing ligand-gated sodium (Na+) channels to open.
The opening of Na+ channels increases the permeability of the motor end plate to Na+ and potassium (K+), leading to depolarization.
If sustained muscle contraction is needed, another motor neuron action potential (AP) releases more Ach.

Agents and Diseases Affecting NMJ Function

Black widow spider venom: Triggers the explosive release of Ach from storage vesicles at all cholinergic sites, including the NMJ.
Curare: Competitively binds to Ach receptor sites on the motor end plate, preventing Ach from binding and opening ion channels. This leads to muscle paralysis.
Acetylcholinesterase (AChE): Destroys Ach before it can bind to receptor sites, reducing the effectiveness of Ach in generating an end-plate potential (EPP).

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Description

Explore the events that occur at the neuromuscular junction, including calcium ion entry and acetylcholine release. Learn about the effects of various agents, such as black widow spider venom and curare, on NMJ function and muscle contraction. Test your understanding of these critical physiological processes.