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PSYC 462 > CH. 5 Catecholamines > Flashcards

CH. 5 Catecholamines Flashcards

1
Q

what does monoamine mean

A

one amine group

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2
Q

what are the types of catecholamines

A

dopamine (DA)
norepinephrine (NE)
epinephrine (EPI)

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3
Q

what is another name for nor/epinephrine

A

nor/adrenaline

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4
Q

where are NE/EPI released from

A

adrenal medulla

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5
Q

what general behavioural functions do catecholamines have

A

motor (DA)
learning and memory
attention
motivation/emotions
reward

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6
Q

what diseases have been linked to dysfunctional catecholamine transmission?

A

parkinson’s
schizophrenia
depression
ADHD
drug addiction

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7
Q

what are the steps of catecholamine synthesis?

A

tyrosine enters the brain
converted to DOPA
converted to DA
converted to NE

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8
Q

what is the enzyme that synthesizes tyrosine to DOPA

A

tyrosine hydroxylase (TH)

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9
Q

what is the enzyme that synthesizes DOPA to dopamine

A

dopamine decarboxylase (AADC)

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10
Q

what is the enzyme that synthesizes DA to NE

A

dopamine beta-hydroxylase (DBH)

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11
Q

what is the rate limiting step in catecholamine synthesis?

A

tyrosine to DOPA step using tyrosine hydroxylase

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12
Q

what precursor would you usually give a Parkinson’s patient who cannot easily produce dopamine? why?

A

DOPA
to skip the slow rate-limiting step

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13
Q

what is the negative feedback loop in catecholamine synthesis?

A

high levels of catecholamines prevent TH activity to synthesize

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14
Q

what effect does increased firing have on TH

A

stimulate to synthesize more catecholamines

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15
Q

L-DOPA function

A

precursor to DA/NE that increases transmitter levels

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16
Q

true or false; only a certain amount of NT can be put into each packaged vesicle

A

false, amount of NT in vesicles can very depending on the condition

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17
Q

AMPT function and effects

A

blocks TH therefore blocks catecholamine synthesis
induces sedation, depression, reduced blood pressure

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18
Q

what drugs can reverse the effects of AMPT

A

L-DOPA

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19
Q

what is the catecholamine vesicle transporter called?

A

vesicular monoamine transporter (VMAT)

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20
Q

what does reserpine do?

A

blocks VMAT

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21
Q

what are the effects of reserpine

A

sedation
depression
reduced blood pressure/heart rate

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22
Q

what enzyme(s) metabolizes catecholamines?

A

monoamine oxidase (MAO)
catechol-O-methyltransferase (COMT)

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23
Q

what is the main DA metabolite

A

HVA

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24
Q

what is the metabolite of NE?

A

MHPG

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25
Q

where can metabolites be found?

A

CSF
bloodstream
urine

26
Q

how are catecholamine metabolites eliminated?

A

through urine

27
Q

example of a MAO inhibitor

A

phenelzine

28
Q

what does phenelzine treat

A

treat clinical depression

29
Q

example of COMT inhibitor

A

tolcapone

30
Q

tolcapone function? effect?

A

prevents COMT degredation of catecholamines
enhances effectiveness of L-DOPA to treat Parkinson’s

31
Q

what feature on catecholamine axon’s allows for volume transmission?

A

varicosities

32
Q

what are varicosities?

A

repeated swellings along an axon filled with NT vesicles

33
Q

what is volume transmission?

A

release of NTs in a ‘mist’ that broadcasts the NT signal farther but less specifically

34
Q

what protein does reuptake of dopamine?

A

dopamine transporter (DAT)

35
Q

what protein does reuptake of noradrenaline?

A

norepinephrine transporter (NET)

36
Q

how selective are the catecholamine transporters?

A

not selective

37
Q

example of how selective catecholamine transporters are?

A

NET is the main transporter of DA in the frontal lobe

38
Q

drugs that affect catecholamine reuptake

A

cocaine
tricyclic antidepressants
methyphenidate

39
Q

cocaine function

A

inhibits reuptake of all monoamines

40
Q

tricyclic antidepressants function

A

inhibits reuptake of NE and 5-HT

41
Q

methyphenidate function

A

inhibit reuptake primarily of catecholamines

42
Q

what do amphetamines do?

A

reverse monoamine transporter/ reverses reuptake

43
Q

what 3 characteristics of amphetamines?

A

independent of cell firing
relatively non selective for monoamines
powerful effects

44
Q

what is an effect of amphetamines we always see

A

increased locomtion

45
Q

what causes the increase in locomotion with amphetamines?

A

increased DA in the nucleus accumbens

46
Q

what happens to locomotion at high doses of amphetamines?

A

replaces by stereotype behaviours

47
Q

what are stereotype behaviours? examples?

A

more localized movement
intense sniffing, sharp head movements, licking, etc

48
Q

why do we see a shift in types of locomotion in lower versus higher doses of amphetamines?

A

amphetamine doses affect different sized areas differently
nucleus accumbens (small area); fully saturated DA release on all neurons at low dose. high dose will not release more
dorsal striatum (bigger area); not fully saturated by lower dose, no observable effect. high dose saturates more neurons and can now over power nucleus accumbens

49
Q

nucleus accumbens function in motion

A

forward motion

50
Q

dorsal striatum function in motion

A

limb/trunk/orofacial movements

51
Q

what is sensitization?

A

repeated exposure of a drug will cause more sensitivity to effects at the same dose

52
Q

another name for sensitization

A

reverse tolerance

53
Q

study demonstrating sensitization

A

1 control and experimental receive same dose of amphetamine and locomotion is measured
2 control receives repeated saline everyday, experimental repeated higher dose
3 both receive original dose amount after 5 days
experimental show significantly increased locomotion

54
Q

therapeutic effects of amphetamines

A

powerful stimulant
cognitive enhancer

55
Q

how are amphetamines powerful stimulants?

A

promote wakefulness

56
Q

how are amphetamines cognitive enhancers?

A

improve attention, working memory, memory encoding

57
Q

how do amphetamines treat ADHD

A

work in the frontal lobe which has a DA deficit
reduce creativity

58
Q

which receptor subtype works as a DA autoreceptor?

A

D2

59
Q

which receptor subtype works as a NE autoreceptor?

A

a2

60
Q

where are monoamine/catecholamine autoreceptors usually located

A

axon terminals
cell bodies

61
Q

how do high and low dose of catecholamine release affect D2/a2 receptors?

A

low; saturates autoreceptors on presynapse therefore reduces locomotion
high; activates a sufficient amount of post synapse receptors to increase locomotion

PSYC 462 (11 decks)

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