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Psych 336: Drug Neuro > exam 2 > Flashcards

exam 2 Flashcards

1
Q

striatum

A

major target of dopamine (DA) axon terminals

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2
Q

major components of brainstem

A

midbrain, pons, medulla oblongota

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3
Q

striatum components and their functional roles

A
  1. nucleus accumbens- pleasure, motivation, reward cues,
  2. caudate- dorsomedial; goal-directed actions; flexible; rapidly acquired behaviors
  3. putamen - dorsolateral; habits, inflexible, automatic behaviors
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4
Q

nigrostriatal pathway

A

substantia nigra –> dorsal striatum
movement and stereotypies

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5
Q

mesolimbic pathway

A

VTA –> ventral striatum (nucleus accumbens) and amygdala

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6
Q

mesocortical pathway

A

VTA –> prefrontal cortex

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7
Q

What is the function of the basal ganglia?
Input and output structures
Output targets

A

voluntary movement, action selection, procedural learning, and habits

Input structure: cortex (glutamatergic - excitatory)
output structures: SNr, GPi (GABAergic- inhibitory)

Targets of output: Thalamus, superior colliculus, PPN

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8
Q

input and output structures of basal ganglia

A

input structures: cortex; glutamatergic (excitatory)
output structures: GPi, SNr; GABAergic (inhibitory)
indirect ptathway

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9
Q

how is dopamine involved (and not involved) in different components of reward learning?

A

not involved: liking
involved in: wanting and reward prediction

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10
Q

what is “reward prediction error” and how is dopamine involved?

A

learning about cues/actions related to reward
positive- increased activity with unexpected reward (activates D1 and DIRECT pathway)
zero- unchanged baseline for expected rewards
negative- decreased activity with unexpected reduction of reward (activates D2 and INDIRECT pathway)

decrease in dopamine firing when an expected reward is omitted

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11
Q

factors that influence addiction vulnerability

A
  1. properties of drug
  2. individual differences (genetic and env.)
  3. drug-induced neuroadaptations
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12
Q

individual differences that increase/protect addiction vulnerability

A

increase:
1. high impulsivity (reduced D2 receptors in striatum)
2. history of trauma/ stress (enhanced habit learning & reduced behavioral inhibition)

protect
1. environmental enrichment
(showed reduced place-preference)

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13
Q

what are the effects of chronic stress?

A
  • enhanced habit learning (DLS)- DLS more dominant than DMS
  • reduced behavioral inhibition (loss of PFC)
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14
Q

what behaviors are associated with prefrontal cortex?

A

self-control; behavioral inhibition; executive function

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15
Q

drug-induced neuroadaptations that increase addiction likelihood

A
  1. enhanced drug motivation (sensitization)
  2. enhanced habit learning (DLS)
  3. reduced behavioral inhibition (PFC) (resistance to neg consequences)
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16
Q

lesions in DMS and DLS

A

DMS- habitual responding
DLS- goal-directed responding

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17
Q

5-HT

A

serotonin

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18
Q

MDMA

A
  • never used clinically
  • can enhance communication and openness
  • club drug during 1980s-90s
  • Schedule 1
  • orally; long half-life (8hrs)
  • effects at low doses: increased energy; increased hr and temp
  • high doses: mild hallucinogenis; hyperthermia; dehydration; stroke; increased hr
  • acute adverse effects: hyperthermia, dehydration
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19
Q

Catecholamine synthesis and inactivation

A

synthesis: tyrosine
inactivation: reuptake via transporters and/or enzymatic degradation (metabolism)

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20
Q

Catecholamine transporters

A

VMAT2 (all have this vesicular monoamine transporter- package into vesicles)

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21
Q

Catecholamine enzymes and metabolites

A

enzymes: MAO (monoamine oxidases), COMT (catechol-o-methyltransferase)

metabolites: 1) dopamine: HVA (humans), DOPAC(rats)
2) Norepinephrine: MHPG

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22
Q

6-OHDA

A

-causes catecholamine lesions
- damages/ destroys catholamniergic neurons

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23
Q

what releases catecholamines?

A

amphetamines

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24
Q

how does cocaine and methylphenydate affect dopamine system?

A

inhibit catecholamine reuptake

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25
Q

Dorsal noradrenergic bundle (DNAB)

A

originates at locus coeruleus in pons

cognition, arousal, attention

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26
Q

ventral noradrenergic bundle (VNAB)

A
  • originates from medullate
  • aversive aspects of stress
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27
Q

what did pharmacological studies show?

A
  • DA antagonists (but not NE antagonists) disrupt amphetamine reinforcement
  • DAT blockage is responsible for reinforcing effects of cocaine and amphetamine
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28
Q

what did lesion studies show?

A
  • Using 6-OHDA to lesion DA affects cocaine reinforcements
  • If destroy dopamine cells in striatum→ don’t get reinforced anymore
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29
Q

what did neurochemical studies show?

A

Repeated amphetamine treatment produces sensitization of locomotor and reinforcing effects, and DA levels in striatum

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30
Q

what did genetic knockout and knockin studies show?

A

knockout: already have high dopamine -> increased locomotion
knockin: showed decreased reinforcement

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31
Q

Stimulant-induced DA in nucleus accumbens (mesolimbic)

A

locomotion & reinforcement

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32
Q

Stimulant-Induced DA in dorsal striatum (nigrostriatal)

A

stereotypies

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33
Q

what does C-raclopride (D2 ligands) binding in addicts show?

A
  • dopamine release
  • binding in dorsal striatum area correlates with craving
34
Q

how do amphetamine, MDMA, and methamphetamines affect DA and 5-HT terminals?

A

amphetamines: damage to DA terminals
MDMA: damage to 5-HT terminals
mehtamphetmaines: damage to both DA and 5-HT terminals

35
Q

nonbenzodiazepines

A
  • “Z drugs”
  • act as benzodiazepine binding site of GABA-A receptor
  • most commonly used for sleep disorders
36
Q

what will intermittent cocaine use followed by abstinence result in?

A

increased potency and drug motivation

37
Q

will rats self-administer when paired with a footshock?

38
Q

addiction

A
  1. compulsive drug seeking
  2. craving
  3. relapse
39
Q

do optogenetic stimulation of PFC make animals resistant to footshock?

40
Q

how do D1 or D2 receptors change in meth abusers?

A

reduced D2 receptor availability

41
Q

T/F: a history of cocaine is correlated with more habitual responding

42
Q

rats with ____ show enhanced place-preference for cocaine

A

social defeat stress

43
Q

____ influences all aspects of the addiction process

44
Q

where are monoamine neuron cell bodies located?

45
Q

why do amph, meth, and MDMA release DA?

A

are agonists of TAAR1 (an intracellular GPCR)

46
Q

what 3 factors play a role in toxicity?

A
  1. Hyperthermia
  2. Reactive oxygen species
  3. High extracellular dopamine
47
Q

what kind of drugs are Antischizophrenia drugs?

A

D2 antagonists

48
Q

which antagonists are not readily self-administered or abused?

A

NET
SERT
Na+

49
Q

which drugs are disguised as bath salts?

A

methcathinone and mephedrone

50
Q

all monoamines have the same __________________ but their own __________________ and __________________

A

same: vesicular transporter
own: synaptic transporters and receptors

51
Q

T/F: DA and NE antagonists will disrupt the reinforcement quality seen during self-administration tests

52
Q

neurotoxicity for amphetamine/meth occurs at doses ________________________________ the normal dose, while MDMA is ________________________________

A

amphetamine/meth: 10-50x
MDMA: 2x

53
Q

what are symptoms of Parkinson’s?

A
  1. bradykinsea
  2. akineseia
  3. drug-induced dyskinesea
  4. slow movement, or complete loss of movement
54
Q

what is DA critical for in effects of amphetamine and cocaine?

A

reinforcing and locomotor

55
Q

when was the peak use of speed?

56
Q

Direct vs indirect basal ganglia pathway

A

Direct: to GPi, SNr; excites targets
Indirect: to GPe, STN; inhibits targets

57
Q

amphetamine treatment sensitizes

A

locomotor and reinforcing effects, and DA in the striatum

58
Q

how do barbs affect sleep?

A

reduce REM and reduce deep sleep

59
Q

what increased the abuse of alcohol?

A

spread of distillation

60
Q

Benzo competitive antagonist

A

Flumazenil

61
Q

ADH vs ALDH

A

affect individual variation in blood levels
ADH: of alcohol
ALDH: acetaldehyde

62
Q

first barbiturates and benzos on the market

A

barbs: barbital and phenobarbital
benzos: Valium

63
Q

how is GABA made?

A

from glutamate
via GAD enzyme

64
Q

medical uses for barbs

A

anesthesia, epilepsy, sedation

65
Q

GABAa subunit required for benzos to have a:
1) rewarding effect
2) anxiolytic effect

A

rewarding: alpha 1
anxiolytic: alpha 2

66
Q

do barbs and benzos bind to the same site on the same receptor?

67
Q

are benzos direct agonists?

68
Q

medical use of benzos

A

anxiolytics, treatment of alcohol withdrawl, anticonvulsant, surgical sedation/ amnesia

69
Q

which GABA receptor is metabotropic with 2 subunits?

70
Q

how is tolerance seen with chronic alcohol use?

A
  • increased ADH
  • induction of cytochrome P450 family liver enzymes
  • behavioral
  • pharmacodynamic
  • cross tolerance with benzos and barbs
71
Q

is overdose of barbs the same cause of death as alcohol?

72
Q

what are characteristics of fetal alcohol syndrome?

A
  • low birth weight
  • low brain weight
  • craniofacial malformation
  • neurological issues
73
Q

how much greater is the risk of alcoholism if you are a relative of an alcoholic?

74
Q

why did benzos replace barbs?

A

benzos have low addiction potential and zero overdose risk

75
Q

what positively and negatively modulates GABAa receptor?

A

positive: benzos
negatively: B-carbolines (found in ayahuasca)

76
Q

what affects variance in duration of different benzos?

A

depot binding and whether metabolites are active or inactive

77
Q

what kind of receptor is GABAa?

A

ionotropic
allows influx of Cl-

78
Q

what are pharmacotherapy alcohol treatment option?

A
  • ALDHD inhibitors
  • mu opioid receptor antagonist
  • partial NDMA antagonist
79
Q

what benzo is used as a date rate drug?

80
Q

why are benzos used to treat chronic alcohol withdrawl?

A

cross-dependence

81
Q

what kind of amnesia do benzos cause?

A

anterograde

82
Q

what is the current medical use for GHB?

A

narcolepsy/ cataplexy

Psych 336: Drug Neuro (2 decks)

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