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LF261: Neuropharmacology > Lecture 5. Nicotinic Receptors of the Neuromuscular Junction & Autonomic Ganglia > Flashcards

Lecture 5. Nicotinic Receptors of the Neuromuscular Junction & Autonomic Ganglia Flashcards

1
Q

What competitively blocks reuptake of choline?

A

Hemicholinium 3

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2
Q

What is reuptake of choline dependent on?

A

Na⁺

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3
Q

What synthesises ACh from precursors choline and Acetyl Co-A from mitochondria?

A

Choline acetyltransferase (ChAT)

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4
Q

What selectively inhibits ChAT?

A

Nothing, recent evidence suggests that it may be inhibited by amyloid proteins seen in Alzheimer’s disease

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5
Q

What inhibits uptake and storage of ACh in synaptic vesicles?

A

Vesamicol

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6
Q

What does tetrodotoxin (TTX) block?

A

Voltage-gated Na⁺ channels (no action potential - no release)

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7
Q

What blocks P/Q & N-type voltage-gated Ca²⁺ channels?

A

Various toxins eg conatoxins (no Ca²⁺ influx - no release)

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8
Q

What does botulinum toxin block?

A

Vesicle fusion - no release

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9
Q

What do dendrotoxins block?

A

Voltage-gated K⁺ channels (more Ca²⁺ influx - more release)

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10
Q

What does ziconotide act as?

A

A selective N-type voltage-gated calcium channel blocker

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11
Q

How is ziconotide given and what is it used for?

A

Given via the intrathecal route for the management of severe pain

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12
Q

What does synaptotagmin detect?

A

Increase in intracellular calcium

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13
Q

What is black widow spider venom?

A

α-latrotoxin (α-LTX)

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14
Q

What happens to the synapses when exposed to α-LTX?

A

Massive ACh release which causes muscle spasms

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15
Q

What happens to the synapses after being exposed to α-LTX?

A

Depletion of vesicle pool
Desensitisation of neuromuscular junction
Inhibition of endocytosis
Distended terminal
Paralysis

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16
Q

What is the effect of an α-LTX dimer?

A

Enhances calcium ion intake into the synapse

17
Q

What is the effect of an α-LTX tetramer?

A

Forms calcium ion channel in the synapse

18
Q

What does the release of each quanta of transmitter at a NMJ give rise to?

A

A miniature end plate potential (mEPP) via activation of nAChRs

19
Q

What do mEPPs summate to give?

A

An end plate potential (EPP), which, if large enough, can initiate an action potential and hence muscular contraction

20
Q

What terminates the activation of nicotinic ACh receptors at NMJ?

A

Acetylcholinesterase (AChE/AChase)

21
Q

What drugs inhibit AChE?

A

Anticholinesterases (eg nerve agents, neostigmine)
Increase the concentration and effects of ACh - can lead to muscle spasms

22
Q

What is tubocurarine?

A

Competitive non-depolarising blocker (antagonist)
Arrow poison - kills prey by respiratory paralysis

23
Q

What are the clinical side effects of tubocurarine?

A

Decreased BP due to ganglion block & resultant vasodilation

24
Q

What are the names of the two competitive non-depolarising blockers in clinical use?

A

Vecuronium & Rocuronium (few side effects)

25
Q

Is vecuronium or rocuronium rapid in onset?

A

Rocuronium

26
Q

What are all competitive non-depolarising blockers reversed by?

A

Anticholinesterases eg neostigmine

27
Q

What occurs in phase I block?

A
  1. Persistent activation of endplate nicotinic - receptors by suxamethonium
  2. Prolonged depolarisation of endplate
  3. Inactivation of voltage-gated sodium channels
28
Q

What occurs in phase II block?

A
  1. Desensitisation of endplate nicotinic receptors
  2. Repolarisation of endplate
  3. Receptor desensitisation maintains blockade
29
Q

What is suxamethonium?

A

Depolarising blocker (agonist)
Used clinically
Rapid onset of paralysis
Short duration – broken down by plasmacholinesterases
Tracheal intubation, electroconvulsive therapy

30
Q

What are the side effects of suxamethonium?

A

Bradycardia (decreased heart rate) due to M2 mAChR activation in heart
K⁺ release in trauma (eg burns) – cardiac dysrhythmias & cardiac arrest
Prolonged paralysis (2hr+) in 1:3500 people

31
Q

What do ganglion blockers do?

A

Reduce the actions of both the sympathetic and parasympathetic nervous systems

32
Q

At the neuromuscular junction, what does the activation of nicotinic receptors promote?

A

Skeletal muscle contraction and underpins physical movement and breathing

33
Q

What can drugs that block nicotinic neuromuscular transmission be used for?

A

Can be used in surgery to prevent unwanted muscular contractions, but by two different mechanisms

34
Q

What can drugs that block nicotinic receptors at the autonomic ganglia be used for?

A

Lowering blood pressure

LF261: Neuropharmacology (15 decks)

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