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PSYC3030 > Acetylcholine > Flashcards

Acetylcholine Flashcards

1
Q

The function of AChE is to

a. help transmission proceed smoothly at the neuromuscular junction
b. break acetylcholine into choline and acetic acid
c. metabolize excess acetylcholine in the terminal button
d. all of the above

A

d. all of the above

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2
Q

Which statement regarding muscarinic receptors is false?

a. They are widely distributed in the brain
b. They are metabotropic
c. They can open potassium channels, causing inhibitory effects
d. They all inhibit the formation of cAMP

A

d. They all inhibit the formation of cAMP

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3
Q

Describe the synthesis of acetylcholine.

A

Choline + acetyl CoA -choline acetyltransferase-> Acetylcholine

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4
Q

What is the name of the protein which stores ACh into vesicles? Where does this happen?

A

ACh is stored in vesicles at axon terminals by vesicular ACh transporters (VAChT)

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5
Q

Describe the breakdown of ACh.

A

Acetylcholinesterase breaks down ACh to choline and acetic acid.

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6
Q

Where does AChE act, and why?

A

In presynaptic terminal to metabolize excess ACh.
In postsynaptic membrane to break down ACh after release.
At neuromuscular junction to allow for efficient contraction.

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7
Q

What is responsible for the reuptake of ACh?

A

Choline transporter takes back up choline for synthesis at the cholinergic nerve terminal

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8
Q

What are the two types of receptors for ACh?

A

Nicotinic and muscarinic

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9
Q

Describe nicotinic receptors, their mechanism, their composition, and their function.

A

Ionotropic receptors which allow Na+ and Ca2+ to flow. They mediate fast excitatory responses in the CNS and PNS. They are composed of 5 subunits.

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10
Q

Describe the mechanism and function of muscarinic receptors.

A

Metabotropic receptors which stimulate K+ channel opening.

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11
Q

What is the role of M5 receptors?

A

M5 receptors contribute to the excitatory effect on DA neurons mediated by nicotinic receptors involved in reward of abused drugs.

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12
Q

Where is ACh used in the sympathetic and parasympathetic nervous systems?

A

SNS: preganglionic neurons only
PSNS: preganglionic neurons and ganglionic neurons

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13
Q

Name 3 areas where ACh acts.

A

Striatum, basal forebrain cholinergic system, and dorsolateral pons.

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14
Q

How does ACh act in the striatum?

A

There are interneurons that regulate movement dependent on the balance of ACh and DA.

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15
Q

Describe the structures where ACh is found in the basal forebrain cholinergic system. What areas does the BFCS innervate?

A

Neurons in nucleus basilis, substantia innominata, medial septal nucleus, diagonal band nuclei.

BFCS innervates the cerebral cortex, hippocampus, and other limbic system structures.

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16
Q

What areas comprise the dorsolateral pons, and what is the role of ACh here?

A

Laterodorsal and pedunculopontine tegmental nuclei.

Excitatory influence on midbrain DA firing.

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17
Q

Which type of receptors are activated by ACh of PSNS, and where are they found?

A

Peripheral muscarinic receptors.

They are found in cardiac muscle, smooth muscle, and beta cells.

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18
Q

Which receptors, specifically, are found in cardiac muscle and what is their function?

A

Cardiac muscle has M2 receptors.

Stimulation of PSNS slows heart rate and decreases contraction strength.

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19
Q

Which receptors, specifically, are found on smooth muscle and what is their function?

A

Smooth muscle has M3 receptors.

Their activation results in contraction.

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20
Q

What is the function of ACh in the striatum?

A

Motor system

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21
Q

What is the function of ACh in the basal forebrain?

A

Memory and cognitive functions

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22
Q

What is the function of ACh in the dorsolateral pons?

A

Sleep and arousal

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23
Q

What happens to mice with no choline transporter? Why?

A

Die within an hour because a lack of ACh synthesis/release at neuromuscular junctions causes breathing difficulties

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24
Q

How do drug reactions change with M5 receptor knockout mice?

A

There is deficit in morphine and cocaine reward

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25
Q

What happens when mice are pretreated with propranolol then given nicotine? What does this suggest?

A

There is no nicotine enhancement of cognitive function. This suggests that beta receptors are necessary for cognitive enhancement

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26
Q

What happens when mice are pretreated with prazosin then given nicotine? What does this suggest?

A

There continues to be a nicotine enhancement of cognitive function. This suggests that alpha receptors do not play a role in cognitive enhancement

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27
Q

What happens to B2 subunit (for nicotinic receptors) knockout mice? What does this suggest?

A

There is a loss of nicotine-mediated DA activation and IV self-administration. This suggests a role of the B2 subunit in nicotine reinforcement.

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28
Q

What happens to a5 subunit (for nicotinic receptors) knockout mice? What does this suggest?

A

Increased dose of self-administration. a5 have a role in the aversive effects of nicotine.

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29
Q

How are acetylcholine levels affected in Alzheimer’s Disease?

A

Low levels of acetylcholine in hippocampus and cell loss in the basal forebrain.

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30
Q

How can Alzheimer’s Disease be treated?

A

Inhibit AChE

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31
Q

What does vesamicol do?

A

Blocks VAChT and reduces the amount of ACh released when the neurons fire

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32
Q

How does Black Widow Spider Venom function? What are the side effects? Is it fatal?

A

Overactivity of cholinergic system in PNS due to ACh release.
Muscle pain, tremors, nausea, vomiting, salivation, copious sweating.
Rarely fatal

33
Q

What does botulism toxin do? Is it fatal?

A

Inhibits ACh release. It can be deadly because of muscle paralysis

34
Q

What does hemicholinium-3 do?

A

Blocks choline transporter, reducing the rate of ACh production.

35
Q

What can AChE inhibitors be used for? How?

A

Alzheimer’s disease.

Increase ACh levels to compensate for cholinergic neuron loss

36
Q

What is physostigmine and what can it treat?

A

Reversible AChE inhibitor that can be used for glaucoma when administered topically. If administered systemically, crosses BBB and bad side effects

37
Q

What are neostigmine and pyridostigmine and what can they treat?

A

Reversible AChE inhibitors that can treat myasthenia gravis.

38
Q

What are organophosphorus compounds?

A

Irreversible AChE inhibitors. Can be used in insecticides if weak versions.

39
Q

How do nerve gases function? What are 2 examples? What side effects may occur?

A

Accumulate ACh and overstimulate cholinergic synapses through CNS and PNS.
Sarin and Soman.
Muscle paralysis and death by asphyxiation.

40
Q

What does succinylcholine function as, and how does it do this?

A

Muscle relaxant.
Causes a depolarization block as a nicotinic agonist. Resting potential is lost and the cell cannot be excited again until the agonist is removed

41
Q

How is succinylcholine function affected by AChE?

A

It is resistant, so it will not be broken down in synapse like ACh

42
Q

What does D-tubocurarine do? What is the result?

A

It is a nicotinic antagonist with a higher selectivity for muscle nicotinic receptors. Leads to muscle paralysis

43
Q

What are muscarine, pilocarpine, and arecoline? What are the side effects?

A

They are muscarinic agonists and parasympathomimetic agents.
Lacrimation, salivation, sweating, pinpoint pupils, severe abdominal pain, painful diarrhea, cardiovascular collapse, convulsions, coma, death

44
Q

What are atropine and scopolamine? What are their side effects?

A

Muscarinic antagonists and parasympatholytic agents.

Toxic when taken systemically, and dilate pupils when applied to eyes.

45
Q

When was nicotine domesticated?

A

5000 years ago

46
Q

When was nicotine first isolated?

A

1828

47
Q

What methods are used to consume nicotine?

A

Smoking, chewing, snorting, vaping

48
Q

How much nicotine does a cigarette contain? How much nicotine reaches the bloodstream?

A

6-11 mg.

1-3 mg.

49
Q

How does nicotine enter the body?

A

Enters the lungs on tar, which readily passes through absorbent surface of lungs to the bloodstream.
To a lesser extent, can enter through mouth/nostrils

50
Q

What are some factors affecting plasma nicotine levels after use?

A

Nicotine concentration of cartridge, rate of puffing, puff duration

51
Q

What enzyme metabolizes nicotine? Where? What is the result?

A

Cytochrome P450 2A6 in the liver. Metabolized to cotinine

52
Q

What is true about those with low CYP2A6 activity?

A

They are less likely to become smokers

53
Q

What is the mechanism of action of nicotine?

A

It activates nicotinic cholinergic receptors.

High doses leads to persistent activation of nAChRs and continuous depolarization

54
Q

What is the biphasic effect of nicotine?

A

Stimulation of nicotinic cholinergic functions, then a nicotinic receptor block

55
Q

How does nicotine affect the behaviour of smokers? Non-smokers?

A

In smokers, produces a calm or relaxed state, partly as relief from nicotine withdrawal symptoms.
In nonsmokers, elicits heightened tension/arousal, along with lightheadedness, dizziness, and nausea.

56
Q

How does smoking (not necessarily nicotine) affect behaviour?

A

Decreases negative affect

57
Q

How does nicotine affect cognition?

A

Enhances performance on cognitive/motor tasks. Conners’ Continuous Performance Test shows that nicotine increases selective attention in low-attention individuals.

58
Q

Which nAChRs play a role in cognitive enhancement?

A

High-affinity nAChRs (a4 and B2 subunits) play a more important role in hippocampal-dependent cognitive enhancement than low-affinity nAChRs (a7 subunit)

59
Q

What subunits are correlated with high-affinity nAChRs?

A

a4 and B2 subunits

60
Q

What subunit is associated with low-affinity nAChRs?

A

a7 subunit

61
Q

How are tolerance and dependence to nicotine observed in mice?

A

Through continuous exposure via osmotic minipump under skin

62
Q

When do mice given continuous exposure to nicotine experience withdrawal?

A

If pump runs out of nicotine or if nicotinic antagonist (e.g., mecamylamine) is given

63
Q

Who is most likely to be susceptible to reinforcing effects of nicotine?

A

Female adolescents

64
Q

What pathway plays a key role in reinforcement of nicotine?

A

Mesolimbic DA pathway (VTA to NAcc).

High affinity nicotinic receptors in VTA stimulate burst firing of DA neurons, increasing DA release in NAcc

65
Q

VTA nicotinic receptors for reinforcement contain primarily which subunits?

A

a4 and a6

66
Q

In humans, polymorphisms for a4, a6, and B2 nicotinic receptor subunits are linked to what?

A

Subjective effects, smoking rates, and risk for developing nicotinic dependence

67
Q

What role do nicotinic receptor a5, a3, and B4 subunits play?

A

Nicotine’s aversive properties, reducing the propensity to consume or self-administer

68
Q

What are the three stages of nicotine reinforcement?

A

Wanting, craving, and needing

69
Q

Where are nicotinic receptors abundant

A

In the autonomic nervous system

70
Q

What can smoking activate? What is the result?

A

Activate SNS and PSNS.

Causes tachycardia and elevated BP (increasing the risk for cardiovascular disease)

71
Q

How does smoking affect appetite?

A

Reduces appetite and increases metabolic rate, resulting in weight loss

72
Q

How can accidental poisoning from nicotine occur?

A

Swallowing, contact with tobacco in field, or insecticides (can be fatal)

73
Q

What happens to nicotine tolerance overnight?

A

It dissipates

74
Q

Describe acute nicotine tolerance.

A

One is mores sensitive to nicotine at the beginning of the day.
This is related to desensitization of central nAChRs, including those that mediate reinforcement

75
Q

Describe chronic nicotine tolerance.

A

Subjective effects (rewarding and aversive) are most susceptible to chronic tolerance. It is slow to dissipate. The primary mechanism is through to be nicotinic receptor desensitization

76
Q

What happens after chronic exposure to nicotine?

A

Chronic exposure elicits compensatory response.

Up-regulation of high-affinity nAChR expression (neuroimaging and postmortem binding)

77
Q

How does one avoid nicotine withdrawal?

A

Smoking must occur repeatedly throughout the day, and mild withdrawal occurs during the night.

78
Q

What is complex abstinence syndrome? What is it mediated by?

A

Affective symptoms, somatic symptoms, and cognitive symptoms that are short-lived.
It is mediated by resensitization of nAChRs, reduced activity of mesolimbic DA pathway, increased CRF signaling in amygdala, and activation of aversion pathway between medial habenula and interpeduncular nucleus.

PSYC3030 (12 decks)

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