NMJ Flashcards

1
Q

what is the function of the NMJ?

A

responsible for transmission of AP from axon to sarcolemma through non-conductive medium

secretes NTs that bind sarcolemma and create EPP

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2
Q

draw a diagram of the NMJ?

A

googel

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3
Q

what is the first process underpinning transmission at the NMJ?

A

loading of ACh into synaptic vessicles by 2ry active transport

H+ pumped into vesicles by H+/ATPase, establishing chemiosmotic gradient for them to flow out again through an antiporter which loads ACh in

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4
Q

how are loaded vesicles moved and where to in the pre-synaptic neuron?

A

pulled along actin filaments of cytoskeleton by motor protein + positioned at presynaptic membrane

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5
Q

what is the role of Ca2+ in the NMJ?

A

when AP arrives at endbulb and depol the membrane, v.g. Ca2+ channels open, Ca2+ influxes

faciliattes fusion of vesicle proteins + presyn membrane proteins

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6
Q

which proteins from the vesicle associate with which proteins from the synaptic membrane?

A

synaptotagmin + synaptobrevin on vesicle assoc with SNAP25 + syntaxin on presyn

SNAP25 coil, forcing proximity

2 membranes can fuse in presence of Ca2+ and cause exocytosis of ACh

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7
Q

what inhibits the process of vesicle fusion with the presyn membrane?

A

botulinum toxin

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8
Q

what is the structure of the post-syn nicotinic ACh receptor?

A

2 alpha, beta, gamma, theta

1 molecule of ACh binds to each alpha subunit, causes conform change creating a channel that allows Na+ and K+ to move in and out respectively

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9
Q

why does the post-syn membrane depolarise if K+ is still moving out?

A

extracellular concentration of Na+ is significantly higher than the intracellular concentration, the influx of Na+ is sufficient to compensate for the loss of positive charge via K+ efflux

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10
Q

how is motor end plate potential ultimately generated?

A

Na+ influx causes many Mini EPPs which sum to increase membrane pot from -90mV to -60mV, when v.g. Na+ channels open, generating sharp spike in depol, and the motor EPP

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11
Q

what receptors are present on the motor end plate in the G1 tract?

A

muscarinic
G protein coupled receptors that use second messenger

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12
Q

how can NT release from vesicles be described?

A

quantal
only whole numbers of vesicles can be released

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13
Q

what happens during hyperpolarisation period?

A

membrane is responsive to stimulations but requires a much higher input to induce AP
(relative refractory period)

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14
Q

how do motor EPPs generate APs?

A

the depolarisation voltage spike caused by the depol (from Na+ entering the cell) of the motor end plate triggers an AP, which propagates down post-syn membrane leading to muscle contraction by opening v.g. Ca2+ channels

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15
Q

what is myasthenia gravis?

A

autoimmune condition characterised by damage to ACh receptors

antibodies bind to receptors + prevent ACh binding, prevent muscle contraction

resp failure: treatment = competitive inhibitors of AChE

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16
Q

what does AChE do?

A

sits in post-syn membrane and catalyses breakdown of ACh to acetate and choline, terminating transmission`

17
Q

what are some inhibitors of AChE?

A

irreversible: sarin
causes involuntary painful muscle contractions that can be fatal

18
Q

what is AChE made from?

A

acetyl CoA from the Krebs cycle
choline (available from diet)