CH. 5 Catecholamines Flashcards

(61 cards)

1
Q

what does monoamine mean

A

one amine group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the types of catecholamines

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is another name for nor/epinephrine

A

nor/adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

where are NE/EPI released from

A

adrenal medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what general behavioural functions do catecholamines have

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what diseases have been linked to dysfunctional catecholamine transmission?

A

parkinson’s
schizophrenia
depression
ADHD
drug addiction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the steps of catecholamine synthesis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the enzyme that synthesizes tyrosine to DOPA

A

tyrosine hydroxylase (TH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the enzyme that synthesizes DOPA to dopamine

A

dopamine decarboxylase (AADC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the enzyme that synthesizes DA to NE

A

dopamine beta-hydroxylase (DBH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the rate limiting step in catecholamine synthesis?

A

tyrosine to DOPA step using tyrosine hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the negative feedback loop in catecholamine synthesis?

A

high levels of catecholamines prevent TH activity to synthesize

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what effect does increased firing have on TH

A

stimulate to synthesize more catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

L-DOPA function

A

precursor to DA/NE that increases transmitter levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

AMPT function and effects

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what drugs can reverse the effects of AMPT

A

L-DOPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the catecholamine vesicle transporter called?

A

vesicular monoamine transporter (VMAT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what does reserpine do?

A

blocks VMAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the effects of reserpine

A

sedation
depression
reduced blood pressure/heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what enzyme(s) metabolizes catecholamines?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the main DA metabolite

A

HVA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the metabolite of NE?

A

MHPG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
where can metabolites be found?
CSF bloodstream urine
26
how are catecholamine metabolites eliminated?
through urine
27
example of a MAO inhibitor
phenelzine
28
what does phenelzine treat
treat clinical depression
29
example of COMT inhibitor
tolcapone
30
tolcapone function? effect?
prevents COMT degredation of catecholamines enhances effectiveness of L-DOPA to treat Parkinson's
31
what feature on catecholamine axon's allows for volume transmission?
varicosities
32
what are varicosities?
repeated swellings along an axon filled with NT vesicles
33
what is volume transmission?
release of NTs in a 'mist' that broadcasts the NT signal farther but less specifically
34
what protein does reuptake of dopamine?
dopamine transporter (DAT)
35
what protein does reuptake of noradrenaline?
norepinephrine transporter (NET)
36
how selective are the catecholamine transporters?
not selective
37
example of how selective catecholamine transporters are?
NET is the main transporter of DA in the frontal lobe
38
drugs that affect catecholamine reuptake
cocaine tricyclic antidepressants methyphenidate
39
cocaine function
inhibits reuptake of all monoamines
40
tricyclic antidepressants function
inhibits reuptake of NE and 5-HT
41
methyphenidate function
inhibit reuptake primarily of catecholamines
42
what do amphetamines do?
reverse monoamine transporter/ reverses reuptake
43
what 3 characteristics of amphetamines?
independent of cell firing relatively non selective for monoamines powerful effects
44
what is an effect of amphetamines we always see
increased locomtion
45
what causes the increase in locomotion with amphetamines?
increased DA in the nucleus accumbens
46
what happens to locomotion at high doses of amphetamines?
replaces by stereotype behaviours
47
what are stereotype behaviours? examples?
more localized movement intense sniffing, sharp head movements, licking, etc
48
why do we see a shift in types of locomotion in lower versus higher doses of amphetamines?
*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
nucleus accumbens function in motion
forward motion
50
dorsal striatum function in motion
limb/trunk/orofacial movements
51
what is sensitization?
repeated exposure of a drug will cause more sensitivity to effects at the same dose
52
another name for sensitization
reverse tolerance
53
study demonstrating sensitization
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
therapeutic effects of amphetamines
powerful stimulant cognitive enhancer
55
how are amphetamines powerful stimulants?
promote wakefulness
56
how are amphetamines cognitive enhancers?
improve attention, working memory, memory encoding
57
how do amphetamines treat ADHD
work in the frontal lobe which has a DA deficit reduce creativity
58
which receptor subtype works as a DA autoreceptor?
D2
59
which receptor subtype works as a NE autoreceptor?
a2
60
where are monoamine/catecholamine autoreceptors usually located
axon terminals cell bodies
61
how do high and low dose of catecholamine release affect D2/a2 receptors?
low; saturates autoreceptors on presynapse therefore reduces locomotion high; activates a sufficient amount of post synapse receptors to increase locomotion