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Musculoskeletal > Physiology of the Skeletal Muscle NMJ > Flashcards

Physiology of the Skeletal Muscle NMJ Flashcards

1
Q

What innervates the skeletal muscle?

A

Fast conducting alpha neurons with myelinated axons and cell bodies in the spinal cord, or the brainstem

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2
Q

What does the axon divide into near the muscle?

A

Unmyelinated branches that innervate an individual muscle fibre

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3
Q

What do individual fibres divide into?

A

Multiple fine branches

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4
Q

What forms the chemical synapse with the muscle membrane of the NMJ?

A

Terminal boutons of multiple fine branches

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5
Q

Where are action potentials conducted to, and what do they cause?

A

Arise in cell body and are conducted via the axons to the boutons; causes release of acetylcholine (ACh)

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6
Q

What are the key structural features of the NMJ?

A

Terminal bouton (and surrounding Schwann cell), synaptic vesicles, synaptic cleft end plate region of sarcolemma, thrown into a series of junctional folds

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7
Q

Where are synaptic vesicles located?

A

Await release cluster in active zones (contain ACh)

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8
Q

Where are nicotinic ACh receptors (nAChRs) located?

A

At regions of the junctional folds that face the active zones

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9
Q

What are the key steps of neuromuscular transmission?

A

Synthesis of ACh in cytoplasm of bouton
Uptake of ACh into synaptic vesicles for concentration and storage
Ca2+ dependent release of ACh into synaptic cleft by exocytosis
Brief activation of nAChRs by reversible binding of ACh
Rapid termination of transmitter action by acetylcholinesterase within the synaptic cleft

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10
Q

What transports choline into the terminal?

A

Choline transporter (symport with Na+)

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11
Q

Where is ACh synthesised?

A

In the cytosol from choline and acetyl Co-A by acetyltransferase

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12
Q

What concentrates ACh in the vesicles?

A

Vesicular ACh transporter

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13
Q

What does arrival of the action potential at the terminal cause?

A

Depolarisation
Opening of voltage-activated Ca2+ channels
Ca2+ entry to the terminal

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14
Q

What does Ca2+ cause the vesicles to do?

A

Causes vesicles docked in active zones to undergo exocytosis

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15
Q

What does ACh do once it has diffuses into the synaptic cleft after being released from the vesicle?

A

Activates post-synaptic nAChRs in the end plate region

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16
Q

How many ACh molecules are needed to activate each nAChR?

A

Two ACh molecules

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17
Q

What are nAChRs?

A

Pentamers of glycoprotein subunits [(alpha 1)2 beta 1 delta elsilon] surrounding a central action pore (formed by M2 helices)

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18
Q

What does the pore present in nAChRs contain?

A

A gate that is closed in the absence of ACh, but opens when ACh binds to the exterior of the receptor at the subunit interface

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19
Q

What is a feature of the gate present in nAChRs?

A

Roughly equally permeable to Na+ and K+ but doesn’t conduct anions

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20
Q

What happens when the nAChR gate is open?

A

Simultaneous Na+ influx and K+ efflux

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21
Q

Why is Na+ influx greater than K+ efflux?

A

The driving force of Na+ is greater than that of K+ at resting membrane potential

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22
Q

What is generated by the simultaneous opening of many nAChRs?

A

A depolarising endplate potential (e.p.p)

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23
Q

What does each vesicle of ACh contain?

A

A quantum of neurotransmitter

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24
Q

What does one quantum produce in response to activation of nAChRs at the endplate?

A

The electrical response of one quantum of transmitter is a miniature endplate potential (m.e.p.p)

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25
Q

What do many m.e.p.ps produce?

A

Summate to produce the e.p.p, a graded electrotonic response

26
Q

What does an e.p.p greater than threshold trigger?

A

“All or nothing” propagated action potential that initiates contraction (this always occurs normally)

27
Q

What happens if an e.p.p is less than threshold?

A

Neither elicits action potential not contraction

28
Q

What does the e.p.p. trigger in Na+ channels?

A

Causes opening of voltage-activated Na+ channels, generating an action potential

29
Q

What is the e.p.p?

A

Graded response determined by the number of vesicles released

30
Q

What does one action potential in the motor nerve trigger?

A

One action potential in the muscle (one-to-one coupling) and a subsequent contraction of the muscle fibre

31
Q

What do drugs that reduce the e.p.p to beneath threshold do?

A

Block neuromuscular transmission because no muscle action potential is generated

32
Q

What are muscle action potential needed to do?

A

Needed to propagate the response over the length of the fibre using voltage-activated Na+ channels

33
Q

What does the muscle action potential cause?

A

Contraction due to the release of Ca2+ from the sarcolemma of the skeletal muscle cells

34
Q

Where does the muscle action potential propagate to over the sarcolemma?

A

Into T-tubules

35
Q

What are T-tubules?

A

Invaginations of sarcolemma that dip deeply into muscle cell

36
Q

What are the T-tubules in close opposition with?

A

The sarcoplasmic reticulum

37
Q

What does the action potential arriving at T-tubules trigger?

A

Release of Ca2+ from the sarcoplasmic reticulum, which in turn causes contraction by interacting with troponin associated with myofibrils

38
Q

What is the rapid termination of neuromuscular transmission a result of?

A

Hydrolysis of Ach by acetylcholinesterase to choline and acetate

39
Q

What is acetylcholinesterase?

A

An enzyme associated with the endplate membrane

40
Q

What happens to choline and acetate once they have been produced by hydrolysis of ACh?

A

Choline taken up by choline transporter, acetate diffuses from synaptic cleft

41
Q

How is acetylcholinesterase efficient?

A

Some Ach molecules hydrolysed even prior to transmitter binding to nAChRs, once unbinding occurs virtually all Ach molecules are hydrolysed

42
Q

What is the result of acetylcholinesterase’s efficiency?

A

Rebinding is limited and the e.p.p I terminated within a few milliseconds

43
Q

What are some substances that target acetylcholinesterase?

A

Anti-cholinesterases = reversibly block action of acetylcholinesterase
Insecticides
Nerve gases = act irreversibly

44
Q

What are some symptoms of neuromyotonin (Isaac’s disease)?

A

Cramps, stiffness, slow relaxation (myotonia), muscle twitches (fasiculations)

45
Q

What is the cause of the acquired form of neuromyotonin?

A

Antibodies attack voltage-gated K+ channels in the motor neuron, disrupting function causing hyperexcitability repetitive firing

46
Q

What does the repetitive firing in neuromyotonin cause?

A

Prolonged e.p.p and repetitive action potential discharge in skeletal muscle fibres?

47
Q

How are anticonvulsants used to treat neuromyotonin?

A

Block voltage-activated Na+ channels (e.g carbamazepine, phenytoin)

48
Q

What characterises Lambert-Eaton myasthenic syndrome?

A

Muscle weakness in the limb (very rare and associated with small cell carcinoma of lung)

49
Q

What causes Lambert-Eaton myasthenic syndrome?

A

Antibodies against voltage-activated Ca2+ channels in the motor neuron terminal results in reduces Ca2+ entry in response to depolarisation (also reduced vesicular release of ACh)

50
Q

What are some drugs used to treat Lambert-Eaton myasthenic syndrome?

A

Anticholinesterases (e.g pyridostigmine) = increase the duration of ACh action potential in synaptic cleft
Potassium channel blockers (e.g 3,4-diaminopyridine) = increase release of ACh by prolonging action potential in motor neuron terminal

51
Q

What are the characteristics of myasthenia gravis?

A

Increasing muscle weakness during periods of activity, often weakness of eye and eyelid muscles is a presenting feature

52
Q

What causes myasthenia gravis?

A

Antibodies against nAChRs in the endplate results in the reduction in the number of functional channels and hence amplitude of e.p.p

53
Q

What are some drugs used to treat myasthenia gravis?

A

Anticholinesterases (e.g edrophonium, pyridostigmine) = increase ACh concentration in synaptic cleft
Immunosuppressives (e.g azathioprine)

54
Q

What is botulinum toxin?

A

Extremely potent exotoxin (related to tetanus and diptheria toxins) that acts at motor neuron terminals to irreversibly inhibit ACh release

55
Q

How does botulinum toxin prevent exocytosis of vesicles containing ACh?

A

Enters presynaptic nerve terminal to enzymatically modify proteins involved in docking of vesicles containing ACh

56
Q

What is the prognosis of botulism?

A

Death rate high, recovery takes several weeks, drugs that block acetylcholinesterase are useless as therapeutic agent

57
Q

What are some clinical and cosmetic uses of botulinum toxin?

A

Low dose botulinum haemoglutin complex delivered by IM injection to treat overactive muscles (dystonias)
Used to smooth out age-related wrinkles by paralysing muscles

58
Q

What do curare-like compounds act as?

A

Competitive antagonists of nAChrs = interfere with postsynaptic action of ACh (e.g vecuronium atracurium)

59
Q

How do curare-like compounds affect the e.p.p?

A

Reduce amplitude to below threshold for muscle fibre action potential generation

60
Q

How are curare-like compounds used clinically?

A

Induce reversible muscle paralysis in certain types of surgery

Musculoskeletal (57 decks)

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