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Yr 1 - Nerves & Muscle > Neuromuscular Junction > Flashcards

Neuromuscular Junction Flashcards

1
Q

What does a motor unit consist of?

A

The motor nerve and all the muscle fibres innervated by that nerve

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2
Q

What happens when the motor nerve fires?

A

All the motor fibres within the motor unit contract

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3
Q

What does the size of the motor unit depend on?

A

The function of the muscle (thigh muscles have 1000s compared to smaller muscles)

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4
Q

What is a neuromuscular junction?

A

Site of chemical communication between a motor (nerve) fibre and a muscle fibres.

The neuromuscular junction is analogous to the synapse between two neurones

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5
Q

How is the neuromuscular transmission designed?

A

Every presynaptic AP results in a postsynaptic AP

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6
Q

Describe the journey of the motor nerve cell from the spinal cord to the point where neurotransmission actually occurs

A
  1. Motor fibres leave spinal cord via ventral roots
  2. Axons are myelinated as they pass through CNS and into PNS
  3. Divide to supply thin unmyelinated fibres
  4. Each axon terminates in a ‘bouton’ (swollen end)
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7
Q

What is a ‘bouton’?

A

Point of contact with muscle cell and where neurotransmission actually occurs

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8
Q

What can each thin unmyelinated motor fibre innervate?

A

Several individual muscle fibre cells

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9
Q

Is neuromuscular transmission chemical or electrical?

A

Chemical –> neurotransmitter involved

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10
Q

What happens when AP reaches axon terminal of presynaptic cell?

A

Causes depolarisation of terminal membrane and opening of voltage gated calcium channels (influx)

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11
Q

What is effect of influx of Ca2+ into cell?

A

Triggers release of neurotransmitter chemical from storage vesicles which fuse with synaptic membrane and contents are released into synaptic cleft

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12
Q

How are vesicles before AP arrives?

A

‘Docked’ and ‘primed’ –> kept close to terminal plasma membrane (release is as rapid as possible)

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13
Q

How is the calcium increase localised?

A

Microdomain

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14
Q

What are nAChRs?

A

Nicotinic receptors that respond to the neurotransmitter acetylcholine

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15
Q

Structure of nAChR?

A
  • Each receptor formed from 5 subunits
  • Heteromeric receptor
  • Each subunit formed from 4 transmembrane segments

Basic structure is same in all, but exact combination of subunit types differ

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16
Q

How many ACh binding sites does a nAChR have?

A

2 alpha subunits with ACh binding sites

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17
Q

How many ACh must bind to activate nAChR?

A

2 molecules of ACh must bind to receptor before receptor is activated (one on each alpha subunit)

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18
Q

What is a MEPP?

A

Miniature End Plate Potential

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19
Q

How is ACh released?

A
  • In bursts, or quanta (1 quantum or multiples of 1)

- Can be released as random event (no AP or calcium influx)

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20
Q

What is a MEPP?

A

Depolarisation caused by single quantum of ACh –> causes local depolarisation of around 0.5 mV

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21
Q

What is effect of multiple MEPPs?

A

They are additive –> become end plate potentials (EPPs) which generate AP

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22
Q

ACh only briefly binds to postsynaptic receptors. What happens to ACh following dissociation from receptor?

A

ACh is rapidly hydrolysed by the enzyme acetylcholinesterase (AChE) into Acetate and Choline

Choline is recycled back into the terminal, acetate is lost in circulation

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23
Q

How is ACh formed?

A
  1. Acetate reacts with co-enzyme A –> forms acetyl-CoA

2. Acetyl-CoA reacts with choline –> forms ACh

24
Q

Inside the vesicle, what is ACh coupled to the counter transport of?

A

H+ –> requires H+ gradient which is an active process (H+ down gradient and out of vesicle exchanged for ACh into vesicle)

25
Q

Once filled, reserve vesicles are anchored near the active zone by what?

A

Synapsin –> tethers them to actin filaments

26
Q

What does ACh bind to?

A

Nicotinic receptor (nAChR)

27
Q

What do ACh receptor agonists and antagonists act on?

A

Direct effects on receptor (nicotinic or muscarinic) or indirect effects on enzyme AChE

28
Q

What are neuromuscular blocking agents used for?

A

Used adjectively to anaesthesia to produce paralysis

29
Q

What are the 2 types of neuromuscular blocking agents?

A

Non-depolarising and depolarising

30
Q

What is an example of a non-depolarising competitive nAChE antagonist?

A

Tubocurarine

31
Q

How does a non-depolarising competitive nAChE antagonist work?

A

Competes with ACh for nicotinic receptor binding sites, acts by competitively blocking the binding of ACh to its receptors.

Muscle paralysis occurs gradually

Does not depolarise the motor end plate

32
Q

What are non-depolarising competitive nAChE antagonists reversed by?

A

AChE inhibitors

33
Q

What is the therapeutic use of non-depolarising competitive nAChE antagonist?

A

Surgery, slow onset and long duration

34
Q

What is an example of a depolarising nAChR agonist?

A

Succinylcholine

35
Q

How do depolarising nAChR agonists blocking agents work?

A

Depolarise the motor end plate (depolarise plasma membrane of muscle fibre)

36
Q

How do depolarising nAChR agonists differ from ACh?

A

o Are more resistant to degradation by acetylcholinesterase (enzyme responsible for degrading ACh)
o Therefore, more persistently depolarise the muscle fibres
o Different to ACh which is rapidly degraded and only transiently depolarises the muscle

37
Q

What is the therapeutic use of depolarising nAChR agonist?

A

Surgery, given continuous IV as short acting (minutes)

38
Q

How do acetylcholinesterase inhibitors work?

A

Inhibit the acetylcholinesterase enzyme from breaking down acetylcholine, thereby increasing both the level and duration of action of the neurotransmitter acetylcholine.

39
Q

What are 3 examples of acetylcholinesterase inhibitors?

A

Neostigmine, Edrophonium, Sarin

40
Q

What is sarin?

A

Nerve agent –> leads to widespread dysfunctions throughout body

41
Q

How can the amount of neurotransmitter released be affected?

A
  1. Neuronal sodium channel blockers

2. Calcium channel blockers

42
Q

How can calcium channel blockers affect neurotransmitter release?

A

No calcium conc increase = no vesicle release (prevent presynaptic terminal depolarisation)

43
Q

How do Botulinum and Tetanus toxins affect neurotransmitter release?

A

Reduce the probability of neurotransmitter release by preventing vesicles binding to pre-synaptic membrane

44
Q

What is effect of Botulinum toxin?

A

Cleaves SNARE proteins (SNARE proteins are involved with fusing synaptic vesicles to the plasma membrane)

Cleaving therefore inhibits release of acetylcholine at NMJ and leads to inhibition of neurotransmission

45
Q

Name 2 NMJ disorders

A
  1. Lambert-Eaton Syndrome

2. Myasthenia Gravis

46
Q

Is Lambert-Eaton Syndrome presynaptic or postsynaptic?

A

Presynaptic –> reduced ACh release

47
Q

What is Lambert-Eaton Syndrome?

A

o Rare autoimmune response which inhibits Ca2+ channels and, therefore, reduces ACh release
o About half of patients have small cell lung cancer

48
Q

What is the mechanism of Lambert-Eaton Syndrome?

A

o Antibodies are directed against the voltage-gated calcium channels in the on the presynaptic membrane of the NMJ

  • If these channels don’t open  no influx of calcium into cell  reduced probability of vesicle release
  • Prevents ACh being released from presynaptic terminal and the subsequent stimulation of the postsynaptic terminal which would lead to muscle contraction
49
Q

How can EMG be used to diagnose Lambert-Eaton Syndrome?

A
  • Apply electrical impulses to nerves and measuring the electrical response of the muscle
  • CMAP unusually small but incremental response to repetitive nerve stimulation, normal latency and conduction velocities
    • Administration of rapid burst of electrical stimuli increase CMAP amplitude
50
Q

What is effect of Amifampridine?

A

Drug that blocks K+ channel so action potential duration is increased, so more ACh released

51
Q

Is Myasthenia Gravis presyaptic or postsynaptic?

A

Postsynaptic –> reduced nAChR activation

52
Q

Mechanism by which Myasthenia Gravis works?

A

o Autoimmune response against nAChR’s (postsynaptic receptor)
- There are fewer AChR to bind, so the end plate potentials (EPPs) are smaller
• With smaller EPPs, the ‘safety factor’ is reduced so less chance that the postsynaptic muscle fibres will be activated
- NMJ less responsive to ACh

53
Q

What are women at early age with Myasthenia Gravis afflicted with?

A

Hyperplasia (enlargement of an organ or tissue caused by increase in reproduction rate of its cells, often as an initial stage in the development of cancer)

54
Q

What are men at older age with Myasthenia Gravis afflicted with?

A

Cancer of thymus

55
Q

How is Myasthenia Gravis presented?

A

o Muscle weakness & fatigue
o 2 forms:
- Affects extraocular muscles (any of the 6 small voluntary muscles that pass between the eyeball and the orbit and control the movement and stabilisation of the eyeball in relation to the orbit)
o Repetitive stimulation leads to decrease contractile strength weakness greatest at the end of the day or after exertion

56
Q

How can Myasthenia Gravis be treated?

A
  1. Anticholinesterase –> directed at enhancing transmission

2. Immunosuppression –> corticosteroids

Yr 1 - Nerves & Muscle (11 decks)

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