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PSYC 450 > ch 5-8 > Flashcards

ch 5-8 Flashcards

1
Q

catecholamines

A

hormones made by adrenal glands

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2
Q

monoamines

A

transmitters that possess one amine group

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3
Q

biogenic amines

A

compounds made by living organisms

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4
Q

adrenergic

A

adrenaline/ epinephrine (EPI)

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5
Q

noradrenergic

A

noradrenaline/norepinephrine (NE)

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6
Q

EPI and NE are secreted by…

A

adrenal medulla

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7
Q

dopaminergic

A

dopamine (DA)

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8
Q

synthesis of dopamine/norepinehrine

A

tyrosine –> L- DOPA –> dopamine –> norepinephrine

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9
Q

enzymes required for synthesis (DA, NE)

A

tyrosine hydroxylase (TH), aromatic amino acid decarboxylase (AACD)
for NE, needs dopamine-β-hydroxylase (DBH) too

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10
Q

rate-limiting enzyme (DA,NE)

A

determines overall rate of formation because it is the slowest (e.g. TH)

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11
Q

TH inhibition and stimulation

A

high catecholamine levels inhibit TH (don’t need more), rate of cell firing stimulates TH (more synthesis due to more enzyme activity)

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12
Q

release of catecholamines

A

synaptic vesicles, important for protection from degrading enzymes and predetermining amount required

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13
Q

vesicular monoamine transporter (VMAT)

A

responsible for vesicular monoamine reuptake
VMAT1: found in adrenal medulla
VMAT2: found in brain
blocked by reserpin (DA and NE are no longer protected making levels drop)

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14
Q

when do (catecholamine) vesicles open

A

nerve impulse, but some drugs can cause this effect without needing s nerve impulse (amphetamine, methamphetamine)

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15
Q

release inhibition (catecholamines)

A

by autoreceptors who either;
1. directly reduce Ca2+ influx needed for exocytosis
2. indirectly reduces Ca2+ by shortening duration of APs entering the terminal

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16
Q

tonic release

A

DA released in single-spiking mode

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17
Q

phasic release

A

DA released in burst mode

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18
Q

varicosities

A

in-passing synpases in which the fibers exhibit repeated swellings

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19
Q

drugs on catecholamine autoreceptors

A

agonists: stimulate autoreceptors (inhibit release)
antagonists: stimulate release by inhibiting the inhibitory affects of autoreceptors

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20
Q

DA and NE transporters

A

induce reuptake

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21
Q

DA and NE transporter-blocking drugs

A

increase transmission in the synapse by not allowing reuptake

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22
Q

breakdown of NE

A

catechol-O-methyltransferase (COMT) and monoamine oxidase (MOA-A)

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23
Q

breakdown of DA

A

catechol-O-methyltransferase (COMT) and monoamine oxidase (MOA-B)

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24
Q

metabolites of catecholamines

A

DA:
- homovanillic acid (HVA)
NE:
- 3-methyl-4-hydroxy-phenylglycol (MHPG) in brain
- vanillymandelic acid in PNS

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25
Q

2 cell groups in midbrain

A

A1-A7= NE pathways
A8-A16= DA pathways

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26
Q

DA pathway function

A

from dorsal striatum to substantia nigra facilitates voluntary mvmt

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27
Q

DA pathway lesions

A
  • behavioral dysfunction
  • sensory neglect
  • motivational deficits
  • motor impairment
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28
Q

dopamine deficient mice (DD mice)

A
  • still can produce NE
  • lacked DA whole life
  • dopaminergic neurons werent damaged, just couldnt produce DA
  • all symptoms of lacking DA were fixed momentarily with L-DOPA injection
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29
Q

5 subtypes of DA receptors

A
  • metabotropic (interact with G protein and second messengers
    D1 and D2 are most common
    D1 and D5 are similar
    D2,D3,D4 are similar
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30
Q

D2 receptors

A
  • autoreceptors
  • found on pituitary gland that makes prolactin (activation inhibits prolactin)
  • can influence K+ channels causing hyperpolarization (inhibiting APs)
  • higher affinity for DA than D1
  • decrease cAMP
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31
Q

D1

A
  • increases cAMP
  • lower affinity for DA
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32
Q

dopamine agonists

A

apomorphine: agonist for D1 and D2 (classical stimulant)
SKF 38393: agonist for D1 (self grooming in mice)
quinpirole: increase locomotion

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33
Q

dopamine antagonists

A

suppress exploratory and locomotor behavior
(D2: catalepsy)

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34
Q

NE containing neurons (CNS)

A

pons and medulla, more specifically in locus coeruleus (A6 cell group)
- provides nearly all NE in the forebrain

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35
Q

NE in PNS

A

autonomic actions

36
Q

BBB and NE

A

blood born NE cannot cross BBB
(blood born NE helps EPI with fight or flight response)

37
Q

NE and EPI receptors

A
  • metabotropic
  • mediates NT (NE) and hormonal (EPI) actions of the catecholamines
    a1 and a2
    β1 and β2
38
Q

a1 receptors

A

increase Ca2+ ion sin postsynaptic cells

39
Q

a2 receptors

A
  • located on noradrenergic terminals (autoreceptor)
  • reduces cAMP
  • causes hyperpolarization
40
Q

β1 and β2 receptors

A

increases cAMP

41
Q

synthesis of serotonin

A

amino acid tryptophan
L-tryptophan -> L-5-hydroxytryptophan –> 5-hydroxytryptamine (5-HT)

42
Q

enzymes of serotonin synthesis

A

tryptophan hydroxylase (TPH) and aromatic amino acid decarboxylase (AACD)

43
Q

rate limiting enzyme of serotonin synthesis

A

TPH

44
Q

tryptophan loading

A

administration of pure tryptophan

45
Q

tryptophan- large neutral amino acids ratio

A

modest increase will not have any effect
large increase will positively enhance mood and cognition
extremely high increase will have negative effects

46
Q

release of serotonin

A

released into synapse by VMAT2
-reserpin depletes serotonergic neurons of 5-HT

47
Q

serontonergic autoreceptors

A

control 5-HT release; terminal autoreceptors directly inhibit release, other autoreceptors indirectly inhibit release by slowing down rate of firing

48
Q

5-HT1a receptor

A

somatodenritic autoreceptors

49
Q

5-HT1b and 5-HT1d receptors

A

terminal autoreceptors

50
Q

drugs that stimulate 5-HT release

A

para-chloroamphetamine, fenfluramine, 3,4-methylenedioxymethamphetamine (MDMA)

51
Q

inactivation of 5-HT

A
  • 5-HT transporters (SERT) reuptake (SSRIs block reuptake)
  • metabolized by MOA-A
52
Q

metabolite of 5-HT

A

5-hydroxyindoleacetic acid (HIAA) used as a measure of serontonergic neurons in the brain
(more rapid neuron firing= more 5-HT= more HIAA

53
Q

serotonergic neuron orgination

A

brainstem, projects to all forebrain areas

54
Q

CNS serontonergic neurons

A

found along midline of brainstem (medulla, pons, raphe nuchlei)

55
Q

cell groups (5-HT)

A

B1-B9

56
Q

raphe nuclei (dorsal , median)

A

give rise to most serotonergic fibers in the forebrain

57
Q

dorsal raphe nucleus neuronal firing

A
  • slow, regular (tonic) while awake
  • slower, irregular while asleep
    > almost stops completely during REM
58
Q

phasic firing of 5-HT

A

triggered by activity in excitatory synaptic inputs to the cells (most come from GABA, glutamate, and acetylcholine, sometimes DA, NE and orexin)

59
Q

serotonin receptors

A
  • 5-HT1a, 1b, 1d, 1e, 1f
  • 5-HT2a, 2b, 2c
  • 5-HT3, 4, 5a, 5b (not in humans)
  • 5-HT6, 7
    all are metabotropic except 5-HT3 which is excitatory ionotropic
60
Q

5-HT1a functions

A
  • particularly concentrated in hippocampus, septal area, amygdala, raphe nuclei
  • reduces cAMP
  • increase K+ opening (hyperpolarization)
61
Q

5-HT2a functions

A
  • more in cerebral cortex
  • activate second messenger systems (increase Ca2+ levels)
62
Q

5-HT2a agonist and antagonist

A

agonist: hallucinogenic
antagonist: used for schizophrenia treatment

63
Q

5-HT1b, 1d agonists

A

constricts blood vessels providing relief from migraine symptoms

64
Q

5-HT3 agonists and antagonists

A

agonists: induces vomiting
antagonist: counteracts vomiting and nausea

65
Q

serontonergic lesions

A

5,7-dihydroxytryptamine (5,7-DHT): massive damage to serotonergic axons and nerve terminals in the forebrain yet raphe nuclei cell bodies are usually spared (cannot cross BBB)
- changes in hunger, anxiety, aggresion, pain sensitivity, learning and memory

66
Q

TPH2 knockout

A

leaves serotonergic neurons intact but they chan’t synthesize 5-HT

67
Q

TPH2 knockout effects

A
  • causes almost complete loss of 5-HT in the brain but preserves 5-HT in the bloodstream and peripheral organs
  • can reverse effects w 5-HTP injection
  • reduced body mass, increased mortality, aggresive, impulsive, poor thermoregulation, abnormal respiration but survives gestation and birth (unlike DD mice)
68
Q

5-HT2a involvement in death

A

SIDS and SUDEP

69
Q

hypophagia (reduced food intake) involves what receptors

A

5-HT1b, 2c agonists
5-HT6 antagonists

70
Q

anxiety involves what receptors

A

5-HT1a partial agonists for anti-anxiety
5-HT2a, 2c agonists induce anxiety
5-HT6 partial agonists induce anxiety

71
Q

pain involves what receptors

A

5-HT1a, 1b, 2c, 7 agonists reduce pain
5-HT2a, 4 agonists exacerbate pain

72
Q

learning and memory involves what receptors

A

5-HT1a agonists, 4 partial agonists improves performance in spatial learning and memory
5-HT6 antagonists improves learning and memory

73
Q

serotonin in the gut

A
  • 90-95% of bodily 5-HT is in the gut
  • synthesized by enterochromaffin cells using TPH1 enzyme
  • 5-HT increases when food is ingested
74
Q

5-HT and IBS

A

5-HT3 partial agonists can treat IBS-C and IBS-D symptoms
5-HT4 helps with IBS-C
5-HT7 slows peristaltic activity

75
Q

synthesis of ACh

A

acetyl CoA + choline –> acetylcholine
- enzyme choline acetyltranferase

76
Q

rate of synthesis of ACh

A

controlled by amount of reactants present/available and cell firing

77
Q

release of ACh

A

vesicular transporter VAChT
- can be blocked by vesamicol (decreases cytoplasm ACh)

78
Q

vesicular blocker vesamicol (ACh)

A

actual exocytosis process doesnt change, only amount of ACh available within the vesicles decreases

79
Q

animal and bacterial toxins and release of ACh

A

dramatically affected

80
Q

overactive ACh

A

muscle pain in abdomen/chest, tremors, nausea, vomiting, salivation, sweating

81
Q

inhibited ACh

A

muscle paralysis

82
Q

inactivation of ACh

A

acetylcholinesterase (AChE) breaks it down into acetic acid and choline
- found inside presynaptic, postsynaptic cell, neuromuscular junctions

83
Q

choline reuptake

A

choline transporter
- drugs that block choline transporters decrease ACh production by inhibiting choline reuptake

84
Q

drugs blocking AChE

A

prevent inhibition of ACh creating an excess
- sometimes used mildly for alzheimers, and glaucome treatment (applied directly to eyes)

85
Q

physostigmine

A
  • AChE inhibitor
  • synthetic analogs do not cross BBB
  • reversible AChE inhibitors

PSYC 450 (4 decks)

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