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The moving animal - Gateway > Innervation and excitation of muscle > Flashcards

Innervation and excitation of muscle Flashcards

1
Q

How is an action potential terminated?

A

Chemical synapses
Electrical synapses (gap junctions)
Neuromuscular junctions

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2
Q

What direction does information cross the synaptic cleft?

A

Only one direction

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3
Q

What is the somatic nervous system?

A

Includes all of the nerves that serve the skeletal muscles and exterior sense organs, inc. skin
Innervates the skeletal muscles

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4
Q

What are atrophic muscles?

A

More adipose tissue

  • 40% fewer fibres
  • 22% atrophy of type 2 fibres
  • fibre type grouping
  • 40% fewer MUs
  • 49% larger MUs
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5
Q

What is a neuromuscular junction?

A

Junction between terminal of a motor neurone and a muscle fibre

  • one type of synapse
  • specialised structures on surface of skeletal muscle
  • motor end plate regions - folds that increase contact area
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6
Q

How does synaptic transmission occur at chemical synapses?

A

Arrival of an action potential

  1. Calcium influx mediated by voltage gated Ca2+ channels
  2. SV sense this rise (Ca2+ binding site and fuses with the plasma membrane)
  3. SV are retrieved back to synaptic terminal
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7
Q

What is Acetylcholine?

A

Neurotransmitter in NMJ
Neurons that synolnesize release Ach and are termed cholinergic
Synthesised from choline and acetyl-CoA§

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8
Q

What are the steps in neuromuscular transmission?

A
  1. Nerve action potential
  2. Ca2+ enter pre-synaptic terminal
  3. Release of Ach terminal
  4. Diffusion of Ach across cleft
  5. Binding of Ach on the post-synaptic receptors
  6. Ach breakdown
  7. Opening of Na+/K+ channels
  8. Post-synaptic membrane depolarisation
  9. Muscle action potential
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9
Q

Describe the quantal release of Ach

A

4 Ca2+ act co-operatively to release one quantum = 1 vesicle (about 10,000 Ach)
Each nerve impulse can stimulate the release of 100 quanta (10^6)
Stimulation of a motor nerve releases a large quantity of Ach which binds to Ach receptors, causing <200,000 Ach receptors to open simultaneously

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10
Q

What is the nicotinic receptor and describe its structure?

A

Membrane spanning protein that specifically binds Ach

  • formed by 5 protein subunits (2𝛂, 𝛃, Δ, ϵ for the mature form)
  • channel and binding site for Ach are on the alpha subunits
  • ligand-gated cation channel
  • activation leads to a net influx of Na+
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11
Q

What is the EPP (end plate potential)?

A
  • net influx of Na+ ions produces a depolarising synaptic potential
  • amplitude EPP is very large (70mV), this change in potential is large enough to rapidly activate the voltage gated Na+ channels in the junctional folds - converts EPP into an AP which propagates along the muscle fibres
  • large number of Ach-gated channels at end-plate ensures synaptic transmission proceeds with high safety factor
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12
Q

What is the muscle action potential?

A

Action potential in normal skeletal muscle cell is similar to the action potential in neurons
- in typical nerve action potential duration is about 1ms
- in skeletal muscle = 2-5ms
- resting potential prior to activation -90mV
_ conduction velocity is roughly 5m/s

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13
Q

What is the sarcolemmal action potential?

A
  1. Release of Ca2+ from sacroplasmic reticulum initiated by AP
  2. Ca2+ binds to troponin which changes shape removing blocking action of tropomyosin, actin active sites exposed
  3. Contraction, myosin crossbridges attach to actin and detach, release of energy by ATP
  4. Removal of Ca2+ by active transport
  5. Contraction ends and muscle fibre relaxes
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14
Q

How is Ach inactivated?

A

Breakdown of Ach is vital in determining efficiency of one-to-one translation of motomeurone APs to muscle APs

  • Ach = Choline and acetate
  • rapid hydrolysis of Ach (1-2ms) ensures brief duration of action
  • Choline re-uptake
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15
Q

What is the safety factor?

A

Ability of neuromuscular transmission to remain effective under various physiological conditions and stresses

  • amount of NT released per nerve impulse increased than required to trigger an action potential in the muscle fibre
  • in normal adult mammals safety factor generally 3-5
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16
Q

Give examples of drugs that act at NMJ

A
  1. Pre-synaptic toxins = botulinum toxin + tetanus toxin (prevent release of Ach by inhibiting exocytosis)
  2. Non depolarising neuromuscular blockers = curane, turbocurarine, pancuronium (antagonist of nicotine receptors)
  3. Depolarising neuromuscular blockers = suxamethonium (agonists of nicotinic receptors, produce depolarisation)
  4. Reversible antiacetylcholineesterases = Physoscigmine (prolong Ach action at post-synaptic receptors)
  5. Irreversible antiacetylcholineesterases = organophosphorus pesticides, sarin gas (phosphorylate Ach)
17
Q

What are non depolarising blocking agents?

A

NM blockers which do not depolarise the motor end plate - clinical use

  • muscle relaxants used adjunctively to anesthesia to produce paralysis for surgery, hypotension and tachycardia
  • reversed by acetylcholine, inhibitor drugs, competitve antagonsists @ Ach receptors
  • tucocurarine not widely used
  • pancuronium, 2nd of 3 drugs used in the lethal injection in US
18
Q

What are depolarising blocking agents?

A

Work by depolarising plasma membrane for muscle fibre, similar to Ach, also degraded by acetylcholinesterase
- have prolonged effects under the influence of Ach esterase inhibitors
- succinylcholine (suocamethonium) in clinical use
two phases:
- 1. depolarising phase, causes muscular fasciculation, whilst depolarising fibres
-2. desensitising phase, muscle is no longer responsive to Ach released by motor neurones

19
Q

What are anticholinesterases?

A

Irreversible anticholinesterases = organophosphorus pesticides, sarin gas (phosphorylate Ach), phosphorylated enzymes are stable and long lived
Antidote = pralidoxime, reactivates AchE by removing phosphate groups

20
Q

What is Myasthekia Gravis?

A

Autoimmune disease in which circulating antibodies block muscle ACH receptors (80% cases)

  • failure of end plate to effectively activate muscle fibre
  • muscle weakness and fatiguability
  • eye muscle weakness
21
Q

What is lambert - eaton syndrome?

A

Rare autoimmune disease, in which circulating antibodies are formed against presynaptic voltage hated channels Ca2+ often associated with cancer (60%)

  • decrease in ACH to be released in synapse
  • weakness from LES typically involves muscles of proximal arms and legs
  • immune mediated
22
Q

What are congenital myastenic syndromes?

A

Family of inherited neuromuscular disorders, characterised by weakness and easy fatiguability
Mutations in gene that encodes for the muscle AchR and AchR-clusterin protein Rapsyn

23
Q

What is a AchE deficiency?

A

Inherited loss of AchE, mutations in gene that encodes AchE

  • autosomal recessive
  • congenital mediated

The moving animal - Gateway (19 decks)

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