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Physiology and Pharmacology > Skeletal Neuromuscular Junction > Flashcards

Skeletal Neuromuscular Junction Flashcards

1
Q

What do neurotransmitters cause at skeletal NMJ?

A

Excitation

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2
Q

What are the 5 steps involved in neurotransmitter release?

A

1) Synthesis of neurotransmitter by enzymes
2) Storage and packaging of neurotransmitter
3) Release of neurotransmitter n calcium channel of the nerve terminal
4) Activation of postsynaptic receptors
5) Inactivation by reuptake

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3
Q

What are the two types of drugs and toxins that act on the synapse?

A

Agonists that activate and antagonists that block

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4
Q

How do drugs enhance synaptic transmission directly?

A

By direct stimulation of post-synaptic receptors by natural transmitters or analogues

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5
Q

How do drugs enhance synaptic transmission indirectly?

A

By increased transmitter release or inhibition of transmitter removal.

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6
Q

How do drugs inhibit synaptic transmission?

A

By blocking synthesis, storage or release from the pre-synaptic neurone or by blocking post synaptic receptors.

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7
Q

What is the action of agonists?

A

They bind to specific receptors and cause a conformational change.

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8
Q

Which drug type has both affinity and efficacy?

A

Agonists

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9
Q

What is efficacy?

A

The ability of agonists to initiate a biological response once it’s bound to a receptor.

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10
Q

What is affinity?

A

The ability of an agonist to bind to a receptor

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11
Q

How do agonists and antagonists interact?

A

Antagonists compete with agonists for binding sites

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12
Q

Do antagonists activate receptors?

A

No

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13
Q

Which drug type has affinity but not efficacy?

A

Antagonists

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14
Q

How is antagonist blocking reversed?

A

By increasing agonist concentration

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15
Q

What determines whether an agonist or antagonist binds?

A

Relative affinity and agonist concentration

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16
Q

How are synapses classified?

A

According to the neurotransmitter released from the presynaptic membrane

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17
Q

What is the classification of synapses that release ACh?

A

Cholinergic

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18
Q

How are the receptors that bind ACh classified?

A

As cholinoreceptors

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19
Q

What are the two classes of cholinoreceptors?

A

Nicotinic and Muscarinic

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20
Q

What activates nicotinic receptors?

A

ACh or nicotine but not muscarine

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21
Q

What activates Muscarinic receptors?

A

ACh and muscarine but not nicotine

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22
Q

Which is faster; Muscarinic or nicotinic receptors?

A

Muscarinic

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23
Q

What kind of receptor is a muscarinic receptor?

A

G-protein coupled receptor

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24
Q

What is the structure of the nicotinic receptor?

A

5 subunits surrounding a pore which forms an ion channel. There are 2 specific ACh binding site on he extracellular surface

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25
Q

What change occurs in the nicotinic receptor following binding?

A

The pore opens rapidly and cations pass through

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26
Q

What is the purpose of the patch clamp technique?

A

Allows recording of activity of a single receptor

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27
Q

How does the patch clamp technique work?

A

Negative suction is applied to the part of the cell where the receptor is present. The currents produce by the flux of sodium ions is measured.

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28
Q

What is the binding characteristic of a-bungarotoxin?

A

It binds irreversibly to nicotinic receptors

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29
Q

What happens when an electrode is inserted into a skeletal muscle synapse?

A

It reads varying potential values

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30
Q

What are mepps ?

A

Miniature end plate potentials

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31
Q

What triggers mepps?

A

ACh release from a single vesicle

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32
Q

What results in a mepp?

A

When activated nicotinic cation channels open and a flux of sodium ions occurs.

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33
Q

What lab technique can be used to reveal vesicles in the act of exocytosis?

A

Microscopy

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34
Q

What species produces a-latorotoxin - a-LTX?

A

Black widow spiders

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35
Q

What does a-LTX initiate?

A

Spontaneous transmitter release

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36
Q

What are the physiological effects of a-LTX on exposure?

A

Massive ACh release and muscle spasms

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37
Q

What are the lasting physiological effects of a-LTX?

A

Vesicle depletion, inhibition of endocytosis, distended terminals and paralysis

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38
Q

What are the 6 stages of nerve stimulation?

A
  1. Presynaptic action potential generated
  2. Synchronous calcium influx via voltage gated channels
  3. Vesicles undergo ACh release
  4. Activation of many nicotinic ACh receptors
  5. Large depolarisation of endplate = EPP
  6. If depolarisation is large enough the postsynaptic voltage gated sodium channels are activated and action potential initiated
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39
Q

What must happen before transmitter release can be studied?

A

The size of the EPP must be reduced

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40
Q

How can EPP be reduced?

A
  • Reducing the calcium flux
  • Magnesium blocks voltage gated calcium channels
  • Buffered saline solution with a higher Mg and lower Ca reduces nerve stimulation
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41
Q

From what does a MEPP result?

A

A singular vesicle

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42
Q

From what do EPPS result?

A

From multiple vesicles

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43
Q

What is the smallest EPP?

A

The MEPP

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44
Q

What is the Quantal Content?

A

The number of vesicles released on average per nerve stimulation.

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45
Q

What is the calculation for the Quantal Content?

A

Q.C. = Mean EPP amplitude (mV)/mean MEPP amplitude (mV0

46
Q

What triggers MEPPs?

A

They are spontaneous

47
Q

What triggers EPPs?

A

Motor nerve stimulation

48
Q

what happens to MEPPs upon nerve stimulation?

A

They summary to give an EPP

49
Q

What happens after an EPP is produced?

A

An action potential arises and causes muscle contraction.

50
Q

How is ACh synthesised?

A

By choline acetyl transferase (CAT) from Acetyl coenzyme A and choline

51
Q

What happens to the choline from the breakdown of ACh by acetate?

A

It is reabsorbed into the synapse

52
Q

What blocks choline transport?

A

Hemocholinum 3

53
Q

What does blocking result in?

A

A decrease in the amount of available ACh for vesicles. This results in decreased EPP and MEPP.

54
Q

What blocks transport of ACh into vesicles?

A

Vesamicol

55
Q

What effect does Vesamicol have on the Q.C.?

A

It has no effect as there is less ACh in each vesicle so the amplitude of he EPP and MEPP decrease in parallel

56
Q

What step in nerve stimulation in affected by the toxin Tetrodtoxin?

A

Release of neurotransmitter

57
Q

What species produces tetrodotoxin?

A

Bacteria in the organ of puffer fish

58
Q

What is the effect of tetrodotoxin?

A

Blocks the voltage gated sodium channels of the action potential. This prevents an action potential occurring which in turn blocks the EPP and so causes paralysis.

59
Q

At what stage of nerve stimulation does conotoxin have an effect?

A

Release of neurotransmitter

60
Q

What species produces conotoxins?

A

Cone snails

61
Q

What is the physiological action affect of conotoxin?

A

It blocks the voltage gated calcium channels. This decreases calcium influx which decreases transmitter release. The EPP decreases whereas there is no change in the MEPP and so the Q.C decreases

62
Q

What indicates that conotoxin works presynaptically?

A

A decrease in the Q.C.

63
Q

What stage of nerve stimulation is dendrotoxin involved in?

A

Neurotransmitter release

64
Q

What species produces dendrotoxin?

A

The green mamba

65
Q

What is the action and effect of dendrotoxin?

A

It blocks the voltage gated potassium channels which prolongs the action potential. It increases the probability the calcium channel will open and so increases the amount of calcium entering. This increases vesicular fusion and transmitter release.

66
Q

What effect does dendrotoxin have on the Q.C?

A

It increases the EPP and as no effect on the MEPP giving an overall increase in the Q.C.

67
Q

What has a similar physiological action to dendrotoxin?

A

4-aminopyridine

68
Q

What stage of nerve stimulation is botulinum toxin involved in?

A

Neurotransmitter release

69
Q

What species produces botulinum toxin?

A

Clostridium botulinum

70
Q

What is the physiological action of botulinum toxin?

A

It enters the nerve terminal and cleaves vesicular proteins involved in exocytosis. The action potential occurs but the vesicle can’t fuse. This decreases neurotransmitter release and leads to respiratory paralysis.

71
Q

How is the Q.C affected by botulinum toxin?

A

The EPP decreases but there is no change in the MEPP and so the Q.C decreases.

72
Q

How is botulinum toxin used clinically?

A

To treat muscle disorders such as chronic migraines, excessive underarm sweating and neuropathic pain.

73
Q

What is an organ bath?

A

A technique used for studying drugs that involves holding a dissected nerve from a rodent in a physiological salt solution and recording twitch-tension.

74
Q

What is tubocurarine’s clinical use?

A

It is a muscle relaxant and so use to cause muscle paralysis during surgery to avoid unwanted muscle contractions

75
Q

What is used to aid in patient recovery after surgery where tubocurarine was required?

A

Artificial respiration or an anticholinesterase like neostigmine.

76
Q

What is the physiological effect of tubocurarine?

A

It is a competitive receptor antagonist that competes with ACh for binding sites and results in muscle paralysis

77
Q

How is neostigmine used to overcome the effects of tubocurarine?

A

It blocks ACh esterase and so the ACh has a longer lifetime in the synaptic cleft increasing its chances on binding to the receptor.

78
Q

How do non-depolarising neuromuscular blockers work?

A

By binding to nicotinic ACh receptors so ACh cannot bind. This leads to a decrease in sodium and so a decrease in the amplitude of the action potential.

79
Q

What is an example of a non-depolarising neuromuscular blocker?

A

Tubocurarine

80
Q

What indicates that tubocurarine acts postsynapticly?

A

It shows no effect on the Q.C as both the EPP and MEPP decrease.

81
Q

What is the physiological action of a-bungarotoxin?

A

It binds irreversibly to the ACh receptor and causes an irreversible block and in turn irreversible paralysis.

82
Q

What species produces a-bungarotoxin?

A

The Taiwan banded Krait

83
Q

What indicates that a-bungarotoxin works on the post synaptic membrane?

A

It decreases the amplitude of both the EPP and MEPP so thee is no net effect on the Q.C.

84
Q

Why is it strange that Suxamethonium causes paralysis?

A

It is a selective nicotinic receptor agonist

85
Q

What is the clinical use for Suxamethonium?

A

It is used for rapid tracheal intubation and prevention of violent muscle contraction associated with electro convulsant therapy.

86
Q

What metabolises Suxamethonium?

A

Plasma cholinesterases

87
Q

What results in Suxamethonium having a long life span?

A

It is not broken down by ACh in the synapse

88
Q

What is a phase one block?

A

The drug or toxin repetitively activate receptors and so there is prolonged depolarisation of the membrane potential. Sodium channels become inactive and don’t conduct sodium so a prolonged depolarisation means no action potential arises in the muscle fibre.

89
Q

What is a phase 2 block?

A

Receptors become desensitised which causes depolarisation of the endplate and the receptor desensitisation maintains the blockade

90
Q

What drugs and toxins cause muscle paralysis?

A

Suxamethonium, tubocurarine and a-bungarotoxin

91
Q

What stage of nerve stimulation is cholinesterase involved in?

A

Inactivation

92
Q

What is the action of AChE?

A

It breaks down ACh into acetate and choline

93
Q

What is the action of anticholinesterase and nerve agents?

A

It inhabits AChE

94
Q

Where do “true” AChE work?

A

At cholinergic synapses where they are bound to the post synaptic membrane

95
Q

Where are pseudo-cholinesterase found?

A

In the plasma

96
Q

What inactivates Suxamethonium?

A

Pseudo-cholinesterase

97
Q

What inhibits both true and pseudo cholinesterase?

A

Anticholinesterase

98
Q

What type of drug is neostigmine?

A

An anticholinesterase

99
Q

Does neostigmine have an effect on the Q.C?

A

No as the EPP and MEPP both increase

100
Q

What s the action of anticholinesterase?

A

Prolongs the duration of the EPP and MEPP due to the increased life time of ACh in the synaptic cleft.

101
Q

What does anticholinesterase allow ACh to do?

A

Rebind to the receptor

102
Q

What are the clinical uses of Anticholinesterases?

A

Used to treat myasthenia gravis that is characterised by loss of ACh receptors, muscle weakness and paralysis.

103
Q

What can organophosphate act as?

A

Nerve agents

104
Q

What is the recovery process of a nerve agent attack?

A

New enzymes must be synthesised over a number of weeks.

105
Q

What is the action of atropine that allows it to be used as a treatment against nerve agents?

A

It counteracts the effects of excessive Muscarinic receptor stimulation by ACh.

106
Q

What is the action of oximes that allows it to be used as a treatment for nerve agents?

A

It influences interactions between ACh and organophosphates.

107
Q

What is the downfall of treatment of nerve agent attack by oximes?

A

It results in ageing which leads to insensitivity to treatment.

108
Q

What are the characteristics of the nerve agent Dyflos?

A

It is volatile, non-polar, lipid soluble, rapidly absorbed through mucous membranes and unbroken skin and can cross the blood/brain barrier.

109
Q

What kind of toxins are anticholinesterase used to treat?

A

Non-depolarising skeletal muscle relaxants

110
Q

Which anticholinesterase is used to treat Alzheimer’s disease?

A

Tacrine

Physiology and Pharmacology (7 decks)

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