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PSYC3030 > Serotonin > Flashcards

Serotonin Flashcards

1
Q

A specific marker for serotonin cells is

a. tyrosine hydroxylase
b. AADC
c. MAO
d. tryptophan hydroxylase

A

d. tryptophan hydroxylase

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2
Q

Why might increasing levels of tryptophan in the blood not increase brain serotonin levels?

a. It doesn’t matter how much tryptophan is present, serotonin is made at a constant rate from brain stores of tryptophan
b. Insulin is required for transport of tryptophan across the blood-brain barrier
c. Tryptophan cannot cross the blood-brain barrier under any circumstances
d. Tryptophan competes with other amino acids for transport across the blood-brain barrier

A

d. Tryptophan competes with other amino acids for transport across the blood-brain barrier

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3
Q

All serotonin receptors are ___ except for the ___ receptor, which is ___.

a. metabotropic; 5-HT5B; ionotropic
b. metabotropic; 5-HT3; ionotropic
c. ionotropic; 5-HT1C; metabotropic
d. ionotropic; 5-HT3; metabotropic

A

b. metabotropic; 5-HT3; ionotropic

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4
Q

In mice with a knockout of the tryptophan hydroxylase 2 gene,

a. the circuitry of the serotonergic system (fiber innervation) is normal, despite the lack of serotonin
b. no serotonin can be synthesized in any part of the animal’s body
c. no pharmacological treatment has been found that is able to restore serotonin, even temporarily
d. impulsive aggression is increased compared to wild-type mice

A

d. impulsive aggression is increased compared to wild-type mice

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5
Q

Drugs that act as agonists at 5-HT2A receptors produce a characteristic “head-twitch” response in rodents and ___ in humans.

a. hallucinations
b. unwanted motor responses
c. antischizophrenic effects
d. Parkinsonian symptoms

A

a. hallucinations

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6
Q

Which of the following is/are not primarily used for treating major depression?

a. atypical antidepressants
b. Monoamine oxidase inhibitors (MAO-Is)
c. Selective serotonin reuptake inhibitors (SSRIs)
d. Lithium therapy

A

d. Lithium therapy

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7
Q

What is the major advantage of the second-generation antidepressants over the MAOIs and the TCAs?

a. They are more effective in treating depression
b. They produce different and less harmful side effects than the older medications
c. They are less selective in their action; hence they can be used for a number of conditions
d. They work faster than the older classes of drugs

A

b. They produce different and less harmful side effects than older medications

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8
Q

Describe the synthesis of serotonin.

A

L-Tryptophan -TPH-> 5-HTP -AADC-> 5-hydroxytryptamine

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9
Q

Where are the two versions of tryptophan hydroxylase found?

A

TPH1 in gut and melatonin-secreting cells in pineal gland, and TPH2 in serotonergic neurons

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10
Q

What is the rate of 5-HT synthesis dependent on and why?

A

It is dependent on the dietary ratio of other amino acids to tryptophan. Tryptophan competes with other amino acids to cross the BBB via the large amino acid transporter

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11
Q

What type of vesicles is serotonin stored in?

A

Dense-core vesicles via VMAT2

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12
Q

What are the terminal 5-HT autoreceptors and how do they work?

A

5-HT1B or 5-HT1D.

Directly inhibit 5-HT release.

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13
Q

What are the somatodendritic 5-HT autoreceptors and how do they work?

A

5-HT1A.

Indirectly inhibit 5-HT release by slowing rate of neuron firing.

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14
Q

How is 5-HT inactivated after release?

A

Reuptake by SERT and metabolized via oxidative deamination.

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15
Q

Which enzyme breaks down 5-HT? What is the result?

A

MAO-A.

5-hydroxyindoleacetaldehyde (5-HIAA)

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16
Q

How many subtypes of 5-HT receptors are there?

A

14

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17
Q

How do the 5-HT1(A,B,D,E,F) receptors function?

A

Decrease cAMP by inhibiting adenylyl cyclase

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18
Q

How do the 5-HT2(A,B,C) receptors function?

A

Activate phosphoinositide system and increase calcium

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19
Q

Where is serotonin found?

A

CNS, chromaffin cells in gut, enteric cells, pineal gland to convert to melatonin

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20
Q

What is the primary CNS pathway for serotonin?

A

Dorsal and median raphe nuclei to cerebral cortex

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21
Q

Is the dorsal or medial raphe nuclei more sensitive to neurotoxins?

A

Dorsal raphe is more sensitive

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22
Q

What behaviours does serotonin play a role in?

A

Sleep-wake cycle, motor output, aggressiveness, spatial learning/memory, satiety

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23
Q

How does serotonin firing relate to the sleep-wake cycle?

A

Tonic firing = awake
Irregular firing = slow-wave sleep
Absence of firing = REM sleep

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24
Q

What might phasic activity of serotonin be involved in?

A

Facilitating motor output while suppressing sensory processing and responding to rewards/punishments

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25
Q

What is the connection between serotonin and aggressiveness?

A

Low CNS serotonergic activity is associated with hyperaggressiveness

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26
Q

How does serotonin relate to spatial learning and memory?

A

5-HT1A activation improves performance in spatial learning and memory

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27
Q

What is the role of serotonin in the gut?

A

Higher serotonin in the gut leads to satiety signals

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28
Q

What is the behavioural result of Tph2 knockout mice? What is the cause of this? How can this be fixed?

A

Increase in aggressive behaviour, usually measured by the resident-intruder test. More impulsive, compulsive, and less anxious. Poor social behaviours and thermoregulation.

Complete loss of 5-HT in the brain but preservation of 5-HT in bloodstream and peripheral organs.

Brain 5-HT can be restored temporarily by injecting animals with 5-HTP and carbidopa (an AADC inhibitor that does not cross BBB)

29
Q

What happens to mice lacking SERT?

A

An array of behavioural and physiological abnormalities due to chronic enhancement of serotonergic activity

30
Q

What type of drug slows the development of Alzheimer’s Disease?

A

Chronic 5-HT4 partial agonist

31
Q

Which knockout mice show increased anxiety?

A

5-HT1A

32
Q

Which drug is often used to treat anxiety and depression?

A

Selective serotonin reuptake inhibitors

33
Q

Which receptor agonists increase anxiety-like behaviour?

A

5-HT2A and 5-HT2C

34
Q

How does 5-HT play a role in pain?

A

Processes pain at the level of the spinal cord

35
Q

Which agonists could be used to reduce neuropathic pain?

A

5-HT1A, 5-HT1B, 5-HT2C

36
Q

Which agonists increase neuropathic pain?

A

5-HT2A and 5-HT4

37
Q

Which agonists are currently being developed to treat neuropathic pain?

A

5-HT7

38
Q

What causes IBS-D and how can it be treated?

A

Serotonergic hyperactivity.

5-HT3 partial agonist

39
Q

What causes IBS-C and how can it be treated?

A

Serotonergic hypoactivity.

5-HT3 partial agonists and 5-HT4 agonists

40
Q

How is 5-HT altered in major depressive disorder?

A

Lowered 5-HT

41
Q

Which allele is associated with reduced level and function of SERT?

A

Short allele

42
Q

What is the monoamine hypothesis of depression?

A

Deficiency in 5-HT, NE, and DA. Changes in monoamine concentrations occur soon after drug treatment but clinical antidepressant effect develops slowly

43
Q

What is the glucocorticoid hypothesis of depression?

A

Stress-related neuroendocrine abnormalities and high CRF secretion. When stress is prolonged and intense, glucocorticoid levels remain high, hippocampal neurons are damaged and no longer respond

44
Q

What is the neurotrophic hypothesis of depression?

A

Low BDNF leads to a loss of dendritic branches and spines in hippocampus/PFC and reduced neurogenesis in the hippocampus.
Antidepressants may prevent decrease of BDNF.
BDNF production is dependent on cAMP second-messenger system

45
Q

How does chronic antidepressant treatment affect beta-receptors?

A

Leads to a down-regulation of beta-receptors with chronic antidepressant treatment

46
Q

What treatments are used for depression?

A

MAOIs, Classic Tricyclics, SSRIs, atypical antidepressants, electroconvulsant shock, and TMS

47
Q

What does 5,7-DHT do?

A

Causes terminal degeneration in 5-HT projection areas. However, does not cross BBB

48
Q

What do methamphetamine derivatives do?

A

Kill off 5-HT neurons in high doses

49
Q

What do 5-HT1B agonists, 5-HT2C agonists, and 5-HT6 antagonists do?

A

Cause hypophagia (reduced food intake)

50
Q

What is the mechanism of action of p-chlorophenylalanine (PCPA)?

A

Rapidly competes with tryptophan for substrate binding domain. Causes irreversible inhibition of TPH at one day

51
Q

What is the mechanism of reserpine?

A

Block storage (VMAT2) and depletes brain 5-HT, DA, and NE

52
Q

What does para-chloroamphetamine (PCA) do acutely and chronically?

A

Acutely increases 5-HT, but chronically decreases 5-HT

53
Q

What does fenfluramine treat and how does it do this?

A

Reverses SERT to help treat obesity by appetite suppression

54
Q

What can SSRIs treat? Why are they used more often than classic tricyclics?

A

Depression, anxiety disorders, OCD, obesity, and alcohol use disorder.
SSRIs have fewer side effects than classic tricyclics

55
Q

What does ecstasy (MDMA) do?

A

More potent effect on 5-HT than amphetamines.

Long-term, at high doses, there is a large depletion of 5-HT in the forebrain of animals

56
Q

What can MDMA treat?

A

In low doses, chronic PTSD

57
Q

What do buspirone, ipsapirone, and 8-OHDPAT do?

A

They are agonists of the 5-HT1A receptor.

Buspirone and ipsapirone are used for anxiety.

58
Q

What is WAY100635?

A

An antagonist of the 5-HT1A receptor

59
Q

How does LSD function?

A

Agonist of 5-HT2A receptor.
Activates SNS.
Receptor forms a “lid” over the binding pocket by trapping the drug.
Disrupts the normal rhythmic oscillations in cerebral cortex due to excitation of 5-HT2A receptor-expressing pyramidal neurons in layer 5 of PFC.

60
Q

What can LSD be used to treat (in low doses)?

A

PTSD

61
Q

What are the behavioural effects of LSD?

A

Produce unusual perceptual and cognitive distortions.

In animal models, head-twitch response

62
Q

What is the abuse potential for LSD?

A

No high abuse potential or withdrawal symptoms

63
Q

Do dependence and tolerance occur with LSD use?

A

Dependence occurs in a small number of users if exposed at an early age.
Most produce rapid tolerance with repeated use due to down-regulation of 5-HT2A receptors

64
Q

What are ketanserin and ritanser?

A

Antagonists of 5-HT2A receptors

65
Q

What is the mechanism of clozapine (Clozaril) and risperidone (Risperdal)? What can they be used for?

A

Block 5-HT2A receptors and D2 receptors.

Used for schizophrenia

66
Q

What are the side effects of peyote and mushrooms?

A

Dizziness, nausea, vomiting

67
Q

What are phenethylamines?

A

5-HT2A agonists; hallucinogens

68
Q

How do atypical antidepressants function?

A

CRF receptor antagonism; enhancement of cAMP second-messenger system

69
Q

What is Galanin?

A

A neuropeptide involved in many functions that are “off” with depression

PSYC3030 (12 decks)

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