Physiology of NMJ Flashcards

1
Q

are the axons of motor neurones innervating skeletal muscles myelinated or unmyelinated

A

both starts myelinated then branches into unmyelinted branches near the muscle

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2
Q

what is a terminal bouton

A

end of nerve branch that forms a synapse with the muscle membrane at the NMJ

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3
Q

what causes the release of acetylcholine

A

the conduction of action potentials that arise in the cell via the axon to the boutons

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4
Q

who transmits faster myelinated or unmyelinated

A

myelinated

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5
Q

what is the neurotransmitter of all motor neurones of skeletal muscle

A

acetylcholine (ACh)

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6
Q

what type of motor neurone innervates skeletal muscles

A

alpha

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7
Q

what part of spinal chord does does myelinated alpha neurone arise from

A

ventral body of spinal chord

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8
Q

where does the pre synaptic terminal bouton synapse

A

the endplate region of the skeletal muscle fibre

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9
Q

what surrounds terminal boutons

A

schwann cell

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10
Q

what are the components of the NMJ

A

terminal bouton

surrounding schwann cells

synaptic vessels

synaptic cleft

end plate region of the muscle cell membrane (sarcolemma)

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11
Q

what is the sarcolemma

A

the end plate region of the muscle cell membrane

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12
Q

what is the synaptic cleft

A

the space between neurones at a nerve synapse across which a nerve impulse is transmitted by a neurotransmitter (aka synaptic gap)

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13
Q

what do synaptic vesicles contain

A

ACh

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14
Q

where do synaptic vesicles cluster

A

active zones

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15
Q

where are nicotinic ACh receptors located

A

at regions of the junctional folds that face the active zones

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16
Q

what are the components of ACH

A

choline and acetylCoA (from acetate)

17
Q

when does the release of ACh from vesicles occur

A

when the action potential opens voltage activated Ca++ channel

18
Q

how is choline transported into the terminal

A

choline transporter (symport with Na+)

19
Q

describe the synthesis of ACh

A

happens in cytosol

from choline and acetyl coenzyme A (supplied by mitochondia) by the enzyme choline acetyltransferase (CAT)

20
Q

what concentrates ACh in the vesicles

A

vesicular ACh transporter

21
Q

what does arrival of the action potential at the terminal cause

A

depolarisation and the opening of voltage activated Ca++ channels - this allows calcium entry to the terminal

22
Q

what happens to the vesicles when calcium is released

A

fuse with the presynaptic membrane (exocytosis) causing ACh to diffuse into the synaptic cleft

23
Q

what does the diffusion of ACh in the synaptic cleft do

A

activates post synaptic nicotinic ACh receptors in the muscle endplate region

24
Q

what are nicotinic ACh receptors made of

A

a pentamer of glycoprotein subunits which surround a cation sensitive pore (opens in the presence of ACh)

25
what happens when nicotinic ACh receptors open
Na+ enter the muscle cell whilst K+ exits = depolarisation called the end plate potential (e.p.p)
26
what is the miniature endplate potential
the electrical response to one 'quantum' of transmitter released from a vesicle - summate to produce the e.p.p
27
what does e.p.p do when it exceeds a threshold
triggers the opening of voltage activated Na+ channels which causes a propagated action potential that initiates contraction
28
what type of response is the e.p.p
graded response
29
where does action potential propagate in the skeletal muscle cell
sarcolemma (surface membrane) then enters transverse T tubules
30
what does action potential arriving at T tubule trigger
release of calcium from SR- which in turn causes contraction by interacting with troponin associated with the myofibrils
31
what terminates the action of ACh
acetylcholinesterase- hydrolyses ACh into choline (taken up by choline transporter) and acetate (diffuses from the synaptic cleft)
32
Neuromytonia : what are the symptoms what causes it treatments
cramps, stiffness, slow relaxation, muscle twitches antibodies against voltage activated K+ channels anticonvulsants
33
lambert eaton myasthenic syndrome: symptoms cause treatment
muscle weakness antibodies against voltage activate Ca++ channels anticholinesterases, potassium channel blockers
34
myasthenia gravis: symptoms causes treatment
progressive muscle weakness during periods of activity antibodies against nicotinic ACh receptors anticholinesterases, immunosuppressants
35
what do anticholinesterases do
increase conc of ACh in synaptic cleft
36
what does botox (botulinum toxin) do
acts at motor neurone terminals to irreversibly inhibit ACh release
37
what do curare like compounds do
competitive antagonists of ACh receptors, reduce amplitude of e.p.p used clinically to induce reversible muscle paralysis