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
Q

what happens when nicotinic ACh receptors open

A

Na+ enter the muscle cell whilst K+ exits = depolarisation called the end plate potential (e.p.p)

26
Q

what is the miniature endplate potential

A

the electrical response to one ‘quantum’ of transmitter released from a vesicle - summate to produce the e.p.p

27
Q

what does e.p.p do when it exceeds a threshold

A

triggers the opening of voltage activated Na+ channels which causes a propagated action potential that initiates contraction

28
Q

what type of response is the e.p.p

A

graded response

29
Q

where does action potential propagate in the skeletal muscle cell

A

sarcolemma (surface membrane) then enters transverse T tubules

30
Q

what does action potential arriving at T tubule trigger

A

release of calcium from SR- which in turn causes contraction by interacting with troponin associated with the myofibrils

31
Q

what terminates the action of ACh

A

acetylcholinesterase- hydrolyses ACh into choline (taken up by choline transporter) and acetate (diffuses from the synaptic cleft)

32
Q

Neuromytonia :
what are the symptoms
what causes it
treatments

A

cramps, stiffness, slow relaxation, muscle twitches

antibodies against voltage activated K+ channels

anticonvulsants

33
Q

lambert eaton myasthenic syndrome:
symptoms
cause
treatment

A

muscle weakness

antibodies against voltage activate Ca++ channels

anticholinesterases, potassium channel blockers

34
Q

myasthenia gravis:
symptoms
causes
treatment

A

progressive muscle weakness during periods of activity

antibodies against nicotinic ACh receptors

anticholinesterases, immunosuppressants

35
Q

what do anticholinesterases do

A

increase conc of ACh in synaptic cleft

36
Q

what does botox (botulinum toxin) do

A

acts at motor neurone terminals to irreversibly inhibit ACh release

37
Q

what do curare like compounds do

A

competitive antagonists of ACh receptors, reduce amplitude of e.p.p

used clinically to induce reversible muscle paralysis