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Flashcards in Skeletal neuromuscular junction Deck (17)
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1
Q

____ is the neurotransmitter released at the neuromuscular junction (NMJ).

A

ACh

2
Q

What enzyme is responsible for rapid termination of transmission at the skeletal neuromuscular junction?

A

ACh esterase

3
Q

_____ _______ synthesises ACh from choline and acetyl coenzyme A

A

choline acetyltransferase

4
Q

What channels are open in the motor neurone terminal in response to action potential (depolarisation)?

A

voltage-activated Calcium channels

5
Q

What are the effects of Calcium entry in the motor neurone terminal?

A
  • Fusion of ACh-containing vesicles with presynaptic membrane
  • Resultant release of ACh into synaptic cleft
6
Q

_____ ___ receptors are activated by ACh at the NMJ. These are __/__ channels

A

Nicotinic ACh receptors

Na/K channels

7
Q

ACh binding to the post synaptic receptor induces __ influx, resulting in depolarisation, known as the ____ ____ ____

A

Na influx

end plate potential

8
Q

The electrical response to one quantum of ACh (from one pre-synaptic vesicle) is known as the ___ ___ ____

A

miniature endplate potential

9
Q

Minature end plate potentials summate to produce the ______ _____. If this exceeds the threshold, an ‘all or none’ _____ _____ is triggered.

A

endplate potential.

action potential
-initiates contraction

10
Q

Achieving the threshold by the endplate potential triggers the opening of _____-_____ _ channels.
This allows AP propagation along the length of the muscle fibre.

A

voltage activated Na channels

11
Q

What’s the name of the invaginations of the sarcolemma that enable AP spread to the sarcoplasmic reticulum?

A

Transverse (T) tubules

12
Q

What does the action potential induce at the sarcoplasmic reticulum?

A

release of Calcium

13
Q

What is the cause of the prolonged relaxation period of the skeletal muscle twitch?

A

It takes time for Ca to be reabsorbed and for cross bridges to be released

14
Q

An autoimmune disease with antibodies against voltage-activated K+ channels in the motor neurone, resulting in muscle tiwtches, cramps and stiffness describes…

A

Neuromyotonia

-treatment: anti-convulsants (carbamezepine, phenytoin)

15
Q

Antibodies against voltage-activated Ca2+ channels in the motor neuron terminal results in reduced Ca2+ and thus reduced ACh release, muscle weakness in the limbs describes…

A

Lambert-Eaton Myasthenic Syndrome

-treatment:
anticholinesterases, K channel blockers

16
Q

Progressively increasing muscle weakness during periods of activity, due to antibodies against ACh receptors in the endplate describes….

A

Myasthenia Gravis

-treatment: anticholinesterases, azathioprine

17
Q

Exotoxic inhibition of ACh release from motor neurone terminals describes…

A

Botulin Toxicity