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Physiology and Pharmacology > Neuromuscular junction > Flashcards

Neuromuscular junction Flashcards

1
Q

What happens at the end of the nerve terminal?

A

Release of neurotransmitters

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2
Q

What do neurotransmitters do?

A

Carry the signal across the synaptic cleft (gap between the neuron and the post synaptic effector cell)
- presynaptic nerve terminals -> postsynaptic membrane

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3
Q

What can the neurotransmitter acting on the receptors cause?

A

Excitation or inhibition

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4
Q

What is the neuromuscular junction?

A

The synapse between a neurone and a skeletal muscle fibre

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5
Q

Name the 5 steps that exist within the synaptic transmission at the neuromuscular junction

A 
1- Synthesis
2- Storage (protect and package)
3- Release
4- Activation
5- Inactivation
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6
Q

How can drugs enhance synaptic transmission directly?

A

Direct stimulation of post-synaptic receptors by-

  • the natural transmitter
  • analogues
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7
Q

How can drugs enhance synaptic transmission indirectly?

A
  • Increased transmitter release

- inhibition of transmitter removal

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8
Q

How can drugs inhibit synaptic transmission?

A

1) Blocking synthesis, storage or release from the pre-synaptic neurone
2) Blocking postsynaptic receptors

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9
Q

What can drugs acting directly on receptors be divided into?

A

Agonists and antagonists

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10
Q

What are agonists and their two impotant properties?

A

Drugs, hormones or transmitters which bind to specific receptors and initiate a conformational change in the receptor resulting in a biological response

Affinity and Efficacy

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11
Q

What is the definition of affinity?

A

The ability of agonists to bind to receptors

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12
Q

What is the definition of efficacy?

A

The ability of an agonist, once bound to a receptor, to initiate a biological response

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13
Q

What do antagonists do?

A

Bind to receptors but do not activate them

Block receptor activation by agonists

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14
Q

What properties do antagonists have?

A

Affinity but not efficacy

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15
Q

What is a competitive antagonist?

A

Competes with the agonist for the agonist binding site on the receptor

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16
Q

What is the neurotransmitter at the NMJ?

A

Acetylcholine

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17
Q

What is the name of the synapses that synthesise and release acetylcholine? What are the receptors incolved called?

A

Cholingeric

Cholinoceptors

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18
Q

What are the two classes on cholinoceptors and what are they activated by?

A 
Nicotinic cholinoceptor (nAChRs) - nicotine
Muscarinic cholinoceptors- muscarine
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19
Q

What is fast synaptic transmission mediated by?

A

Transmitter-gated ion channels

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20
Q

What does Ash released from a vesicle cause?

A

a miniature endplate potential

  • activates many nicotinic ACh receptors
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21
Q

What occurs upon activation of the nicotinic cation channels?

A

They open and Na+ ions flux into the muscle fibre to cause a local depolarisation at the endplate region

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22
Q

What does exocytosis and endocytosis do?

A

Exo- vesicle fusion

Endo- recovery of vesicular membrane after fusion

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23
Q

What is essential for neurally-evoked neurotransmitter release?

A

Localised calcium entry via voltage-gated calcium channels

24
Q

What blocks the voltage-gated calcium ion channel?

A

Magnesium

25
Q

What does a high Mg2+ low Ca2+ extracellular solution result in?

A

Reduces the app to below the threshold for firing an action potential

26
Q

What suggests that the release of a neurotransmitter at the NMJ is quantal?

A

The amplitude of the app is a multiple of the amplitude of the meep, with the smallest epp amplitude equal to that of the mepp amplitude

27
Q

What is the quantal content equation?

A

QC= mean EPP amplitude (mV) / mean MEPP amplitude (mV)

number of vesicles/stimulus

28
Q

How do MEPPs and EPPs occur?

A

MEPPs- occur spontaneuosly without nerve stimulation

EPPs- occur in response to motor nerve stimulation

29
Q

In MEPPs what happens upon nerve stimulation?

A

MEPPs summate to give an end plate potential (EPP) which initiates an action potential -> muscle contraction

30
Q

What occurs in the first step of the synthesis stage?

A

Choline acetyl transferase (CAT) synthesises ACh from precursors choline and Acetyl Coenzyme A from mitochondria

31
Q

What is the reuptake of choline dependant on and blocked by in the synthesis stage?

A

Na+ dependant and blocked competitively by hemicholinium 3?

32
Q

What happens to the amplitude of the epp and mepp due t less ACh in each vesicle in the synthesis stage?

A

The amplitude is decreased to a similalr extent ie. n change in quantal content

33
Q

What is a Tetrodotoxin (TXX)?

A

A powerful toxin produced by bacteria and concentrated organs of the puffer fish e.g liver

34
Q

What happens when the toxin TXX is exposed to humans? How does it act?

A

Causes paralysis of the diaphragm leading to respiratory failure
Acts like a local anaesthetic lidocaine, much more potent

35
Q

TXX blocks Na+ channels, what does this mean for action potentials and epp?

A

No action potential- no release, no epp

36
Q

What channel does conotoxin block? And what happens to the quantal content when the epp amplitude decreases?

A

Voltage gated Ca+ channels

Decreased quantal content, no change in the mepp ampitude

37
Q

What channel is blocked by the toxin dendrotoxin? And what happens to the quantal content?

A

Blocks voltage-gated K+ channels

Quantal content is increased due to increased mepp and epp amplitude

38
Q

What is the toxin Botulinum used for clinically and cosmetically?

A

Clinically- Treat a variety of muscle disorders, chronic migraine and excessive sweating, neuropathic pain

Cosmetically- Botox

39
Q

How does the toxin Botulinum act?

What happens to the mepp, epp and quantal content?

A

Blocks vesicle fusion by cleaving a vesicular protein required for exocytosis- decreased release

mepp- no change
epp- decreased amplitude
quantal content - decreased

40
Q

What does non-depolarising neuromuscular blockers compete with ACh for?

A

Binding to skeletal muscle nicotinic ACh receptors

41
Q

What do non - depolarising neuromuscular blockers reduce the amplitude of for muscle fibre action potential generation?

A

Reduce amplitude of endplate potential (epp)

42
Q

In amuscle fibre action potential, what happens when there is no action potential?

A

No muscle contraction occurs

43
Q

What is tubocurarine used for?

And what does it allow the surgeon to conduct?

A

Used during surgery to produce skeletal muscle paralysis

Allows surgeon to conduct intricate surgery without the complexity of unwanted skeletal muscle contracion

44
Q

What does the patient require after having tubocurarine? Why?

A

Requires artificial respiration as the diaphragm muscle is also paralysed

45
Q

How is the muscle block that tobocurarine causes, reversed?

A

Anticholinesterases

46
Q

What toxin cant be reversed by washout or anticholinesterases?

A

alpha-Bungarotoxin

47
Q

What is used for rapid tracheal intubation and to prevent violent muscle contraction?

A

suxamethonium

48
Q

Link the NMJ nAChRs to whether they are agonists, competitve antagonist or irreversible antagonist:

  • ACh and nicotine
  • Suxamethonium
  • Tubocurarine
  • a-Bungarotoxin
A

ACh and Nicotine- Agonist
Suxamethonium- Agonist
Tubocurarine- Competitive antagonist
a-Bungarotoxin- Irreversible antagonist

49
Q

How is ACh terminated in the inactivation stage and what is it broken down into?

A

Terminated by an enzyme acetylcholinesterase

Breaks down ACh to acetate and choline

50
Q

What effects do drugs that inhibit AChE have an the effects of ACh?

A

Increase the effects of ACh

51
Q

-Present at cholinergic synapses
- Bound to the postsynaptic membrane in the synaptic cleft
These are characteristics of what?

A

“True” acetylcholinesterase

52
Q
  • Widely distributed and found in plasma
  • Important in inactivating the depolarising neuromuscular blocker, suxamethonium

These are characteristics of what?

A

Pseudo-cholinesterase

53
Q

True or false, both “true” and pseudo cholinesterase’s are inhibited equally by most clinically-relevant anticholinesterases

A

True

54
Q

Name two examples of anti cholinesterase drugs

A

Neostigmine

Edrophonium

55
Q

An example of organophosphate is nerve gas agents such as novichok. How can these be reversed?

A

Atropine

Oximes

Physiology and Pharmacology (22 decks)

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