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Neuro-pharmacology > Acetylcholine > Flashcards

Acetylcholine Flashcards

1
Q

Criteria for Neurotransmitters (NT) 1

A

Presynaptic cell should contain the substance as well as a mechanism to synthesise it

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2
Q

Criteria for Neurotransmitters (NT) 2

A

Substance should be released when depolarizing stimulus is applied to the neuron

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3
Q

Criteria for Neurotransmitters (NT) 3

A

Receptors should be present on the postsynaptic cell

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4
Q

Criteria for Neurotransmitters (NT) 4

A

Known antagonists should block the effects

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5
Q

Criteria for Neurotransmitters (NT) 5

A

A system to inactivate the substance must exist

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6
Q

Criteria for Neurotransmitters (NT) 6

A

Exogenous application of the substance to the postsynaptic cell should produce the same response

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7
Q

Neuromodulators can be

A

hormone-like (acting at a distance)

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8
Q

Autocrine

A

(self-acting)

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9
Q

Juxtacrine

A

(adjacent)

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10
Q

Paracrine

A

(near)

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11
Q

Endocrine

A

(far)

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12
Q

Exocrine

A

outside

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13
Q

Neuromodulators May act at locations

A

other than the synapse

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14
Q

Neuromodulators Does not

A

elicit a direct effect on the postsynaptic cell, but alters the action of a classical neurotransmitter

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15
Q

Neuromodulators May function in

A

anterograde or retrograde manner

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16
Q

Neuromodulators may be

A

released from glial cells

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17
Q

Neurons that use acetylcholine are termed

A

cholinergic neurons

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18
Q

acetylcholine is a

A

Common neurotransmitter at neuromuscular junctions in the periphery

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19
Q

Synthesis of acetylcholine

A

Acetyl-coA + Choline – ChAT—> acetylcholine

20
Q

ChAT is only expressed in the

A

cytoplasm of neurons that use ACh as a neurotransmitter

21
Q

Choline is derived primarily from

A

from hydrolysis of dietary lipids (phosphatidylcholines) by phospholipase D.

22
Q

Choline is

A

is water soluble and is only capable of crossing the BBB due to the presence of specific choline transporters.

23
Q

metabolism of acetylcholine

A

acetylcholine —-AChE—> choline + acetate

24
Q

ACh synthesis is tightly regulated for three reasons

A

Product inhibition
Precursor availability (choline and acetyl-CoA)
Neuron activity (increased during high activity)

25
Q

product inhibition of acetylcholine

A

High levels of ACh in the cell inhibit the synthesis of further ACh by ChAT

26
Q

Precursor availability (choline and acetyl-CoA)

A

Increasing dietary choline has been explored as a treatment for conditions where the cholinergic system has been damaged (e.g. Alzheimer’s) – but not to any significant success

27
Q

Neuron activity (increased during high activity)

A

Activity-dependent synthesis ensures sufficient ACh is available during periods of high activity

28
Q

ACh Storage

A

Stored in vesicles at the nerve terminal by vesicular ACh transporter

29
Q

ACh transport

A

transported by vessicles

30
Q

Transport is inhibited by the drug

A

vesamicol Blocking vesicle transport depletes the pool of release-ready vesicles

31
Q

ACh Re-uptake

A

ACh is broken down in the synapse to attenuate signalling
Breakdown product (choline) transported by choline transporter
Majority of choline is recycled to ACh

32
Q

Re-uptake inhibited by the drug

A

hemicholinium-3

33
Q

Botox

A

Local injection causes muscle paralysis by inhibiting ACh release

34
Q

Insecticides and ACh

A

ACh is a primary neurotransmitter of the insect CNS

35
Q

Plant alkyloids

A

secondary metabolites commonly synthesized for defense against insect or animal predation

36
Q

AChE inhibition

A

prolongs ACh signalling

37
Q

AChE inhibition decreases the rate of

A

ACh breakdown in the synaptic cleft leaving more ACh to act at postsynaptic receptors

38
Q

Plant-derived toxin physostigmine is a

A

BBB permeable inhibitor of AChE (found in Calabar beans

39
Q

Synthetic BBB-impermeable analogues neostigmine (Prostigmin) and pyridostigmine (Mestionon) are used to treat the

A

autoimmune disease myasthenia gravis (MG)

40
Q

Physostigmine, pyridostigmine, and neostigmine are

A

reversible inhibitors of AChE

41
Q

Myasthenia gravis results from

A

immune response to ACh receptors at neuromuscular junctions – attenuating response to ACh signals. Treatment with AChE inhibitors prolongs the ACh signal and compensates for the lost function.

42
Q

malathion

A

inhibit AChE irreversibly

43
Q

Sarin and VX

A

nerve gas) are irreversible AChE inhibitors

44
Q

Pyridostigmine prescribed as

A

preventative agent to nerve gas poisoning

45
Q

Pyridostigmine later found to have increased BBB permeability under stress conditions

A

Use linked to one component of Gulf War Syndrome
Confusion-ataxia syndrome
Cognitive impairment, dizziness, balance and coordination problems

Neuro-pharmacology (26 decks)

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