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Second Year - Biomedical Sciences BS22001 > Lecture 1, 2 & 3 - Physiology and Pharmacology of the Neuromuscular Junction > Flashcards

Lecture 1, 2 & 3 - Physiology and Pharmacology of the Neuromuscular Junction Flashcards

1
Q

What allows for communication at the synapse

A

The release of chemical messengers (neurotransmitters)

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2
Q

Where are neurotransmitters released from to allow communication at the synapse

A

The presynaptic nerve terminals

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3
Q

What do neurotransmitter act upon on the post synaptic membrane

A

Receptors

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4
Q

What are the five steps involved in the release of neurotransmitters

A

Synthesis, storage, release, activation and inactivation

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5
Q

What can affect the steps involved with the release of neurotransmitters

A

Drugs and toxins

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6
Q

Why are neurotransmitters stored

A

For protection and so that the quantity of neurotransmitter released can be controlled

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7
Q

How can drug enhance synaptic transmission

A

By direct stimulation of postsynaptic receptors or by indirect action

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8
Q

What are examples of direct stimulation of synaptic transmission

A

Natural transmitters and analogues

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9
Q

What indirect action causes enhanced synaptic transmission

A

Increasing transmitter release and the inhibition of transmitter removal

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10
Q

How can drugs inhibit synaptic transmission

A

By blocking synthesis, storage or release of neurotransmitter from the presynaptic neurone and by also blocking post synaptic receptors

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11
Q

What are the two different types of drugs that act directly on receptors

A

Agonist and antagonists

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12
Q

What are agonists

A

Drugs, hormones or transmitters that bind to specific receptors and initiate a conformational change

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13
Q

Two important properties of agonists

A

Affinity and efficacy

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14
Q

What is the affinity of an agonist

A

The ability of the agonist to bind to the receptor

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15
Q

What is the efficacy of an agonist

A

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

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16
Q

Since agonists bind and activate receptors they have both

A

Affinity and efficacy

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17
Q

Role of antagonists

A

They bind to receptors but do not activate them

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18
Q

Do antagonists have affinity and efficacy

A

The have affinity but lack efficacy

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19
Q

What is a competitive antagonist

A

It competes with the agonist for the agonist binding site on the receptor

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20
Q

How is a block by an antagonist reversed

A

By increasing the agonist concentration

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21
Q

How are synapses classified

A

By the neurotransmitter released from the presynaptic neurone

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22
Q

What is the classification of synapses where the presynaptic neurone is acetylcholine

A

Cholinergic

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23
Q

What are the receptors upon which ACh acts on known as

A

Cholinoceptors

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24
Q

What are the two classes of cholinoceptors

A

Nicotinic ACh receptors and muscarinic cholinoceptors

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25
Q

What activates nicotinic ACh receptors

A

ACh or nicotine

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26
Q

What activates muscarinic receptors

A

ACh or muscarine

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27
Q

What type of receptor is the nicotinic ACh receptor

A

Transmitter-gated ion channel

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28
Q

How do nicotinic ACh receptors operate

A

An agonist binds to the receptor which induces a rapid conformational change to open the channel. The channel is selective for certain ions and the signalling happens extremely fast.

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29
Q

What are the nicotinic ACh receptors composed of

A

Separate protein subunits

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30
Q

What do the separate protein subunits of a nicotinic ACh receptor form

A

A central ion conducting channel

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31
Q

What do the separate protein subunits in a nicotinic ACh receptor allow for

A

Rapid changes in the permeability of the membrane to certain ions and rapidly alter membrane potential

32
Q

Once the nicotinic ACh receptors are activated what does this also cause the activation of

A

The associated nicotinic cation channels

33
Q

Once the nicotinic cation channels open what moves into the muscle fibre

A

Na+ ions

34
Q

What does an influx of Na+ ions cause in the muscle fibre

A

Local depolarisation at the endplate region

35
Q

What does motor nerve stimulation cause

A

The synchronous release of many vesicles, which causes the summation of MEPPs which go on to produce an EPP

36
Q

What does the EPP cause

A

It depolarises the membrane potential to threshold

37
Q

When the membrane potential is at threshold what is activated

A

Voltage-gated Na+ channels and this induces an action potential

38
Q

How to calculate the quantal content

A

The mean EPP amplitude (mV) ÷ the mean MEPP amplitude (mV)

39
Q

Do MEPPs or EPPS occur spontaneously

A

MEPPs

40
Q

What is required to cause an EPP to occur

A

Motor nerve stimulation

41
Q

What synthesises ACh from Acetyl Co-A and choline

A

Choline acetyl transferase (CAT)

42
Q

Within the synapse where does the Acetyl Co-A come from

A

The mitochondria

43
Q

What step is Na+ dependent

A

Reuptake of choline

44
Q

What is the reuptake of choline blocked by

A

Hemicholinum 3

45
Q

What blocks the transport of ACh into vesicles

A

The inhibition of the ACh transporter

46
Q

What inhibits the ACh transporter

A

Vesamicol

47
Q

What is the action of tertrodoxin (TTX)

A

It blocks the Na+ channels so no action potential can be generated

48
Q

What blocks voltage-gated Ca2+ channels

A

Conotoxins

49
Q

When voltage-gated Ca2+ channels are blocked what happens to the quantal content

A

The EPP amplitude decreases but there is no change in the MEPP amplitude so the quantal content decreases

50
Q

What is the action of dendrotoxin

A

It blocks the voltage-gated K+ channel

51
Q

What does the blockage of voltage-gated K+ channels cause

A

A prolonged action potential

52
Q

How does dendrotoxin affect the quantal content

A

The EEP amplitude is increased but there is no change in the MEPP amplitude so the quantal content increases

53
Q

What does botulinum toxin do

A

It blocks vesicle fusion so there is no release

54
Q

How does botulinum toxin affect the quantal content

A

The EPP amplitude decreases and the MEPP amplitude remains the same so the quantal content decreases

55
Q

What effect does turbocaranine have on muscles

A

It is a muscle relaxant

56
Q

What is turbocaranine

A

A competitive non-depolarising neuromuscular blocking agent

57
Q

What is turbocaranine reversed by

A

Anticholinesterases

58
Q

What is alpha-bungarotoxin

A

An irreversible antagonist

59
Q

What is suxamethonium

A

A muscle relaxant with rapid onset and a short duration

60
Q

What is suxamethonium metabolised by

A

PLASMA ( i.e. butyric cholinesterase)

61
Q

What is involved in the phase one block of suxamethonium

A

Persistant activation of endplate nicotinic receptors, prolonged depolarisation of the endplate and the inactivation of voltage-gated sodium channels

62
Q

What is involved in the phase two block of suxamethonium

A

Desensitisation of endplate nicotinic receptor and depolarisation of endplate. The receptor desensitisation maintains the blockade.

63
Q

Is suxamethonium an agonist or antagonist

A

Agonist

64
Q

Where are true acetylcholinesterase found

A

At the cholinergic synapse, bound to the postsynaptic membrane

65
Q

Where are pseudo-cholinesterases found

A

In plasma

66
Q

What are pseudo-cholinesterases important in

A

Inactivating the depolarising neuromuscular blocker, suxamethonium

67
Q

What inhibits both true and pseudo-cholinesterases

A

Anticholinesterases

68
Q

What is neostigmine

A

An anticholinesterase

69
Q

What action does neostigmine have on the quantal content

A

It increases both the amplitude of both the EPP and MEPP so there is no effect on the quantal content

70
Q

What is the function of neostigmine

A

It prolongs the duration of the MEPP and EPP due to the increased life-time of ACh in the synaptic cleft

71
Q

What do anticholinesterases do

A

The inhibit the breakdown of ACh by inhibiting acylecholinesterase

72
Q

What are some clinical uses of anticholinesterase drugs

A

Reversal of neuromuscular paralysis, diagnosis and treatment of myasthenia graves and the treatment of Alzheimer’s disease

73
Q

How is recovery from anticholinesterases achieved

A

A new enzyme has to be synthesised

74
Q

What are dyflos

A

Volatile, non-polar, lipid-soluble molecules

75
Q

What can reverse nerve gas

A

By atropine and oximes

76
Q

What does atropine do

A

It counteracts the effects of excessive muscarinic receptor stimulation by ACh

77
Q

What function do oximes have

A

To reactivate the AChase

Second Year - Biomedical Sciences BS22001 (28 decks)

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