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MSK > Physiology and Pharmocology of Skeletal Neuromuscular Junction > Flashcards

Physiology and Pharmocology of Skeletal Neuromuscular Junction Flashcards

1
Q

describe the cells which innervate skeletal muscle

A

myelinated axons of motor neurones divide into unmyelinated branches near the muscle
these branches then further divide into fine branches which end in a terminal bouton which form a chemical synapse at NMJ of a single muscle cell
each unmyelinated branch supplies one muscle cell

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2
Q

how is an action potential transferred to a muscle cell?

A

AP arises in cell body and conducted along axon to the boutons which causes the release of ACh

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3
Q

where are the cell bodies of motor neurones found?

A

ventral horn of spinal cord or brain stem

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4
Q

where do presynaptic terminals(boutons) synapse with the muscle cells?

A

endplate region

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5
Q

name 4 key features of the NMJ

A
  1. terminal bouton and surrounding schwann cells
  2. synaptic vesicles
  3. synaptic cleft
  4. end plate region of muscle cell membrane (sarcolemma) thrown into junctional folds
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6
Q

what are active zones at the NMJ?

A

where vesicles containing ACh are released

at the surface of the axon terminal

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7
Q

where are nicotinic ACh receptors located?

A

at regions of the junctional folds of the end plate region

face the active zones

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8
Q

what are the 5 stages of synaptic transmission at NMJ?

A 
1 = synthesis of ACh
2 = Storage of ACh in vesicles
3 = release of ACh at active zones
4 = nicotinic ACh receptor activation
5 = transmitter inactivation
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9
Q

how is ACh synthesised?

A

cholins transported into terminal via choline transporter (Na+ symport)
choline combines with acetyl coenzyme A (from mitochondria) in cytosol with help from choline acetyltransferase enzyme

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10
Q

how is ACh concentrated in vesicles?

A

vesicular ACh transporter

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11
Q

how is ACh released from vesicles?

A

arrival of the action potential at the terminal causes depolarization and opening of voltage gated Ca2+ channels allowing Ca2+ entry to the terminal
Ca2+ causes vesicles which are docked at active zones to fuse with presynaptic membrane (exocytosis)
ACh diffuses into the synaptic cleft to activate post synaptic nicotinic ACh receptors in endplate region

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12
Q

what are the pre and post synaptic terminals?

A 
pre = bouton
post = end plate
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13
Q

what are nicotininc ACh receptors made up of?

A

pentamer of glycoprotein subunits which surround a central cation selective pore

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14
Q

how does a nicotinic ACh receptor work?

A

pore contains a gate which is closed when ACh is absent and open when 2 ACh molecules bind to the outside
when gate open - Na+ enters, K+ leaves (equally permeable)

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15
Q

how is an end plate potential created?

A

although equally permeable to both Na+ and K+, the driving force for Na+ is greater than that for K+ at resting potential so Na+ influx exceeds K+ efflux causing a depolarization called the end plate potential

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16
Q

what is a quantum?

A

a specific amount of ACh which is contained and released from all vesicles

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17
Q

what is the electrical response to a quantum of neurotransmitter at the end plate?

A

miniature endplate potential (MEPP)

18
Q

how do MEPPs cause an EPP?

A

many MEPPs due to many vesicles being released summates to an EPP
because the number of MEPPs can vary this means that EPP is a graded response

19
Q

what does an EPP do?

A

depolarizes end plate region enough that a threshold is reached and an action potential is triggered (due to opening of voltage activated Na+ channels)

20
Q

is an AP a graded response?

A

no

all or nothing

21
Q

what causes an EPP?

A

activation of nicotinic ACh receptors in end plate

graded

22
Q

what does a single action potential in a motor neuron cause in a muscle cell?

A

1 AP in motor neuron = 1 AP in muscle = single twitch

23
Q

how can drugs cause muscle weakness/paralysis?

A

can reduce amplitude of EPP so AP is never triggered

24
Q

why are voltage gated Na+ channels required along the muscle cell?

A

without them the electrical event at the end plate would decline as it spread along the muscle and wouldnt excite so contraction could not occur
Na+ channels allow the AP to propagate over whole muscle fibre

25
Q

how does the muscle action potential cause contraction?

A

it spreads over the surface (sarcolemma) and enters transverse (T) tubules which are in close apposition to sarcoplasmic reticulum
AP arriving at the T tubule triggers release of Ca2+ from SR which then causes contraction by binding to troponin etc

26
Q

how do muscle AP and contraction compare in terms of time?

A

AP is very brief, contraction is longer

27
Q

what is the latent period?

A

time between AP and contraction where Ca2+ is being released from SR

28
Q

what is the relaxation period?

A

decreasing strength of contraction as calcium is being reabsorbed into SR

29
Q

what is the contraction period?

A

increasing strength of contraction

30
Q

how is neuromuscular contraction terminated?

A

hydrolysis of ACh by acetylcholinesterase (AChE)

occurs in synaptic cleft

31
Q

what does AChE do?

A

hydrolyses ACh to choline and acetate
choline reabsorbed
acetate diffuses out

32
Q

how is AChE used in drugs?

A

nerve gas and some therapeutic agents block its action causing increased ACh in synaptic cleft and therefore increased contraction

33
Q

what is neuromyotonia and how is it treated?

A

autoimmune disease where antibodies attack K+ channels in motor neurones causing hyperexcitability
treated with anti-convulsants which block Na+ channels

34
Q

what is Lambert Eaton Myasthenic Syndrome and how is it treated?

A

autoimmune disease where antibodies attack Ca2+ channels in motor neurone which causes reduced vesicular release of ACh and hence muscle weakness
treatment includes anticholinesterases (anti AChE) and potassium channel blockers which increase concentration of ACh in synaptic cleft

35
Q

what is myasthenia gravis and how is it treated?

A

autoimmune disease where antibodies attack nicotinic ACh receptors in the end plate causing reduction in amplitude of EPP and threshold therefore not reached
treatment includes anticholinesterases and immunosuppressants

36
Q

what is botulinum toxin?

A

exotoxin that acts at motor neurone terminal to irreveribly inhibit ACh release

37
Q

how does botulinum inhibit ACh release?

A

enters presynaptic terminal to enzymatically modify proteins involved in the docking of vesicles containing ACh at active zone, therefore preventing exocytosis

38
Q

how is botulinum toxin treated?

A

no effective therapy

recovery takes weeks

39
Q

how is botulinum used?

A

can be used in low doses to treat overactive muscles (dystonia) like squints
smoothing out wrinkles (botox)

40
Q

what are crurare like compounds?

A

interfere with postsynaptic action of ACh by acting as competitive antagonists on ACh receptor
reduce amplitude of EPP to below threshold so no AP generated

41
Q

how are crurare like compounds used?

A

clinically to induce reversible muscle paralysis in certain types of surgery

42
Q

what mediates transmission at NMJ?

A

quantal release of ACh which acts on post junctional nicotinic ACh receptors to increase membrane cation conductance generating an EPP

MSK (66 decks)

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