The Neuromuscular Junction

Question 1

How does an action potential lead to the release of actelycholine?

Answer 1

Voltage gated calicum ion channels open, and there is an influx of calcium ions into the cell. Ca2+ binds to syntaptomagnin, the vesicle is brought closer to the membrane, snare complex helps to make a fusion pore, and transmitter is released through the fusion pore.

Question 2

What are the key features of the calcium ion channel?

Answer 2

The alpha or a1 subunit is the perforating subunit, nesscary for the functional channel, and other channel fine tune properties and enable the correct regulation of the channel. Similar to the sodium ion channel, in there are 4 subunits, each split into 4 transmembrane domains.

Question 3

Name some of the key structural features at the neuromuscular junction.

Answer 3

Vessels, mitochondria, junctional folds, acteylcholinesterase in the synaptic cleft.

Question 4

What sort of Ach receptor is found at the neurovascular junction?

Answer 4

Nitconic

Question 5

What happens upon binding of Ach to the nitonic receptor?

Answer 5

Ach binds to the alpha subunit, causing a confirmational change that leads to the opening of the receptor, it produces an endplate potential, which raises the muscle above the thresholds, so an action potential is produced in the muscle membrane

Question 6

What are the two different blockers of nitonic ACh channel?

Answer 6

Competative blockers and depolarising blockers

Question 7

How do depolirsing blockers of the ACh channels work?

Answer 7

They cause a maitained action potential, which failures to activate the the adjacent Na+ channels, which become inactivated

Question 8

give an example of a competitive blocker of the nitonic Ach recptor?

Answer 8

Tubocarine

Question 9

Give an example of a depolarising blocker of the nitconic Ach channel

Answer 9

Succinlycholine

Question 10

What are some of the symptoms of Mysathenia Gravis?

Answer 10

Profound muscle weakness

Question 11

How does Mysatehnia gravis develop?

Answer 11

Antibodies are produced that are directed agansint nAChr on the postsynaptic membrane of skeletal muscle, leading to the loss of function nAChr by complement mediated lysis, and receptor degradation.

Question 12

What happens to action potentials in mysathenia gravis?

Answer 12

Endplate potential is reduced in amplitude, which leads to muscle weakness and faitugu.

Question 13

What causes minture end plate potentials?

Answer 13

Spontaneous release of acetlycholine vesicles

Question 14

What is the other receptor of acteylcholine and how does it differ in function?

Answer 14

The muscarinic receptor which is a g protein coupled receptor

Question 15

What is the value of Eca?

Answer 15

+122 mV