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Neuro-pharmacology > dopamine > Flashcards

dopamine Flashcards

1
Q

catecholamines

A

epinepherine, norepinepherine, dopamine

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2
Q

epinepherine operates in the

A

PNS

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3
Q

Catecholamine

A

neurotransmitters have common structure (with individual variations)

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4
Q

dopamine synthesis

A

L-tyrosine – Tyrosine hydroxylase -> L-DOPA – DOPA decarboxylase -> dopamine

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5
Q

when AMPT attaches to TH what does it do

A

inhibits the synthesis of dopamine, norepinepherine, epineperine

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6
Q

VMAT

A

is the transporter that loads dopamine into synaptic vesicles

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7
Q

Reserpine

A

Reserpine inhibits VMAT and depletes DA and NE as cytosolic catecholamines are rapidly degraded

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8
Q

Reserpine treatment causes

A

sedation in animals and induces depression in humans

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9
Q

intracellular pathway of dopamine

A

dopamine —MAO–> DOPAC — COMPT –> HVA

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10
Q

Extracellular pathway of dopamine

A

dopamine —COMPT–> 3MT — MAO –> HVA

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11
Q

Cocaine and amphetamine affect

A

DAT functions

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12
Q

Cocaine & amphetamines inhibits

A

DAT preventing dopamine reuptake

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13
Q

preventing dopamine uptake causes what ?

A

Increases dopamine in the synapse
Prolongs dopamine signalling
Hyperactivity of dopaminergic circuits

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14
Q

Presynaptic cell rich in

A

anabolic enzymes (TH, DOPA decarboxylase)

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15
Q

VMAT expressed on vesicles for

A

loading dopamine

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16
Q

Dopamine receptors in

A

postsynaptic membrane

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17
Q

Autoreceptors in

A

presynaptic membrane for feedback inhibition

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18
Q

Dopamine transporter (DAT) responsible for

A

reuptake

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19
Q

D1

A

family [D1, D5] – G-protein coupled receptors signalling through Gsα to ↑cAMP (Excitatory)

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20
Q

D2

A

family [D2, D3, D4] – G-protein coupled receptors signalling through Giα to ↓ cAMP (Inhibitory)

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21
Q

Unlike classical synapses, dopamine can often synapse onto the

A

neck of dendritic spines

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22
Q

synapsing onto the neck of dendritic spines

A

allows dopamine to modulate the activity of the synapse

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23
Q

Dopamine can gate the signals at dendritic spines –

A

– increasing or decreasing signal transmission

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24
Q

Dopamine accounts for 90% of

A

catecholamine neurotransmission in the CNS

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25
Q

Nigrostriatal system

A

projects from substantia nigra and ventral tegmental area to striatum (caudate and putamen)

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26
Q

Tuberoinfundibular system

A

projects from the hypothalamus to the medial eminence to stimulate the pituitary
prolactin secretion

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27
Q

Mesolimbic/mesocortical system

A

Projects from the ventral tegmental area to the limbic system, nucleus accumbens, mesial frontal, anterior cingulate, and entorhinal cortex

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28
Q

Dopaminergic lesions Bilateral nigrostriatal lesion

A

sensory neglect, motivational deficits, motor impairment.

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29
Q

Unilateral lesion of nigrostriatal pathway results in

A

postural asymmetry and turning

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30
Q

6-hydroxydopamine (6-OHDA) is a

A

selective neurotoxin.

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31
Q

Nigrostriatal system

A

Projects to the striatum
Involved in motor control
D1 and D2 family receptors
Degradation in Parkinson’s leads to motor symptoms

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32
Q

treatment of parkinsons disease includes

A

includes L-DOPA, precursor to dopamine

33
Q

MPTP

A

) is a neurotoxin that degrades dopaminergic neurons in the Substantia nigra and produces Parkinson’s symptoms and is resistant to L-dopa treatment

34
Q

Degeneration of dopaminergic neurons in the nigrostriatal system

A

central to the pathophysiology of Parkinson’s disease

35
Q

target receptors in parkinsons

A

Targets enriched with D1 and D2 receptors in the basal ganglia

36
Q

DAT knockout causes

A

hyperactivity - Decreased re-uptake prolongs DA signalling at the synapse

37
Q

Cocaine (inhibiting DAT activity) has comparable effects on

A

locomotion to DAT knockout.

38
Q

D1 receptor knockout removes

A

cocaine’s hyperlocomotion

39
Q

Mesolimbic dopaminergic pathways Targets enriched in

A

D1, D2 family receptors

40
Q

Mesolimbic dopaminergic pathways Limbic connections are proposed to

A

mediate memory, learning, and affect

41
Q

Mesolimbic dopaminergic pathways The nucleus accumbens is proposed to act to modify

A

salience of information flow, implicated in motivation & addictions (motivational salience), and psychosis (sensory salience)

42
Q

Schizophrenia and Psychotic disorders positive symptoms

A

Delusions
Hallucinations
Disorganized speech
Grossly disorganized or catatonic motor behaviour

43
Q

Schizophrenia and Psychotic disorders negative symptoms

A

Avolition
Social deficits
Flattened affect
Cognitive deficits

44
Q

Schizophrenia and Psychotic disorders Psychosis proposed to result from

A

altered dopaminergic signalling

45
Q

Hyperactivity in mesolimbic system leads to

A

positive symptoms

46
Q

Nucleus accumbens in SCZ Mesolimbic dopamine is proposed to mediate

A

salience

47
Q

Motivational salience

A

addictions

48
Q

Sensory salience

A

– sensory gating

49
Q

Nucleus accumbens in SCZ Excess dopamine activity leads the patient to

A

perceive voices, sounds, and imagery as inappropriately salient

50
Q

Nucleus accumbens in SCZ - False significance assigned to

A

internal and external stimuli are interpreted as delusions and hallucinations

51
Q

Typical antipsychotics inhibit

A

D1 and D2 family dopamine receptors

52
Q

Chlorpromazine

A

(first discovered neuroleptic)

53
Q

Haloperidol

A

(still widely used front-line antipsychotic)

54
Q

Antipsychotic efficacy is correlated with

A

D2 binding potential

55
Q

Stimulants (esp. amphetamine) can induce

A

psychosis at sufficient dose

56
Q

Extrapyramidal side effects (nigrostriatal):

A

akinesia, akathesia, acute dystonic reaction, Pseudoparkinsonism,

57
Q

Akinesia

A

inability to initiate movement

58
Q

Akathisia

A

inability to remain motionless

59
Q

Acute dystonic reaction

A

– sustained muscle contraction, twisting and repetitive movements

60
Q

Pseudoparkinsonism

A

– fixed (non-progressive) Parkinsonism without degeneration of dopaminergic neurons

61
Q

Extrapyramidal side effects Tuberofundibular:

A

Hyperprolactinaemia

62
Q

Hyperprolactinaemia

A

can result from antipsychotic treatment
Amenorrhea (♀), infertility(♂/♀), sexual dysfunction (♂/♀), hypogonadism (♂), spontaneous lactation (♂/♀)

63
Q

Dopamine levels in post-mortem SCZ brains are

A

are elevated in the striatum

64
Q

SCZ - PET and SPECT imaging of dopamine receptors show

A

show increased basal levels of dopamine

65
Q

Basal dopamine levels are predictive of

A

responsiveness to antipsychotic therapy

66
Q

typical antipsychotics targeting dopamine only address

A

positive symptoms

67
Q

in SCZ what is the dopamine activity in the cortex?

A

hypoactivity of dopamine seen in cortex

68
Q

Gaba neuron is

A

inhibitory – take it away and we lose control

69
Q

Addictive behaviour is linked to

A

impulsive traits in humans

70
Q

Impulse control

A

is a manifestation of inhibitory control (component of executive function)

71
Q

Impulse control Involves structures such as

A

anterior cingulate, dorsolateral prefrontal cortex, lateral orbital prefrontal cortex, and motor/premotor cortex

72
Q

Inhibitory control can be considered a

A

gating event

73
Q

Impulsive rats show increased premature responses and have

A

increased self-administration of cocaine than low impulsive rats (○)

74
Q

PET imaging of a dopamine receptor D2/3 antagonist showed high

A

impulsive rats have reduced binding potential in the ventral striatum.

75
Q

Reduced D2/3 binding potential correlates with high

A

impulsivity and addictive behaviour (cocaine self-administration).

76
Q

SCZ patients have very high comorbidity with

A

addictions

77
Q

Cannabis or amphetamine intoxication is a frequent precipitant of the first

A

episode of psychosis

78
Q

Early substance use / abuse (teenage use) correlates with

A

SCZ onset and severity but is neither necessary nor sufficient

Neuro-pharmacology (26 decks)

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