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Psych 336: Drug Neuro > exam 2 > Flashcards

exam 2 Flashcards

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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
Dorsal noradrenergic bundle (DNAB)
originates at locus coeruleus in pons cognition, arousal, attention
26
ventral noradrenergic bundle (VNAB)
* originates from medullate * aversive aspects of stress
27
what did pharmacological studies show?
* DA antagonists (but not NE antagonists) disrupt amphetamine reinforcement * DAT blockage is responsible for reinforcing effects of cocaine and amphetamine
28
what did lesion studies show?
* Using 6-OHDA to lesion DA affects cocaine reinforcements * If destroy dopamine cells in striatum→ don't get reinforced anymore
29
what did neurochemical studies show?
Repeated amphetamine treatment produces sensitization of locomotor and reinforcing effects, and DA levels in striatum
30
what did genetic knockout and knockin studies show?
knockout: already have high dopamine -> increased locomotion knockin: showed decreased reinforcement
31
Stimulant-induced DA in nucleus accumbens (mesolimbic)
locomotion & reinforcement
32
Stimulant-Induced DA in dorsal striatum (nigrostriatal)
stereotypies
33
what does C-raclopride (D2 ligands) binding in addicts show?
* dopamine release * binding in dorsal striatum area correlates with craving
34
how do amphetamine, MDMA, and methamphetamines affect DA and 5-HT terminals?
**amphetamines**: damage to DA terminals **MDMA**: damage to 5-HT terminals **mehtamphetmaines**: damage to both DA and 5-HT terminals
35
nonbenzodiazepines
* "Z drugs" * act as benzodiazepine binding site of GABA-A receptor * most commonly used for sleep disorders
36
what will intermittent cocaine use followed by abstinence result in?
increased potency and drug motivation
37
will rats self-administer when paired with a footshock?
yes
38
addiction
1. compulsive drug seeking 2. craving 3. relapse
39
do optogenetic stimulation of PFC make animals resistant to footshock?
no
40
how do D1 or D2 receptors change in meth abusers?
reduced D2 receptor availability
41
T/F: a history of cocaine is correlated with more habitual responding
true
42
rats with ____ show enhanced place-preference for cocaine
social defeat stress
43
____ influences all aspects of the addiction process
stress
44
where are monoamine neuron cell bodies located?
brainstem
45
why do amph, meth, and MDMA release DA?
are agonists of TAAR1 (an intracellular GPCR)
46
what 3 factors play a role in toxicity?
1. Hyperthermia 2. Reactive oxygen species 3. High extracellular dopamine
47
what kind of drugs are Antischizophrenia drugs?
D2 antagonists
48
which antagonists are not readily self-administered or abused?
NET SERT Na+
49
which drugs are disguised as bath salts?
methcathinone and mephedrone
50
all monoamines have the same __________________ but their own __________________ and __________________
**same**: vesicular transporter **own**: synaptic transporters and receptors
51
T/F: DA and NE antagonists will disrupt the reinforcement quality seen during self-administration tests
False
52
neurotoxicity for amphetamine/meth occurs at doses ________________________________ the normal dose, while MDMA is ________________________________
amphetamine/meth: 10-50x MDMA: 2x
53
what are symptoms of Parkinson's?
1. bradykinsea 2. akineseia 3. drug-induced dyskinesea 4. slow movement, or complete loss of movement
54
what is DA critical for in effects of amphetamine and cocaine?
reinforcing and locomotor
55
when was the peak use of speed?
1970s
56
Direct vs indirect basal ganglia pathway
Direct: to GPi, SNr; excites targets Indirect: to GPe, STN; inhibits targets
57
amphetamine treatment sensitizes
locomotor and reinforcing effects, and DA in the striatum
58
how do barbs affect sleep?
reduce REM and reduce deep sleep
59
what increased the abuse of alcohol?
spread of distillation
60
Benzo competitive antagonist
Flumazenil
61
ADH vs ALDH
affect individual variation in blood levels **ADH**: of alcohol **ALDH**: acetaldehyde
62
first barbiturates and benzos on the market
**barbs**: barbital and phenobarbital benzos: Valium
63
how is GABA made?
from glutamate via GAD enzyme
64
medical uses for barbs
anesthesia, epilepsy, sedation
65
GABAa subunit required for benzos to have a: 1) rewarding effect 2) anxiolytic effect
rewarding: alpha 1 anxiolytic: alpha 2
66
do barbs and benzos bind to the same site on the same receptor?
no
67
are benzos direct agonists?
no
68
medical use of benzos
anxiolytics, treatment of alcohol withdrawl, anticonvulsant, surgical sedation/ amnesia
69
which GABA receptor is metabotropic with 2 subunits?
GABA B
70
how is tolerance seen with chronic alcohol use?
* increased ADH * induction of cytochrome P450 family liver enzymes * behavioral * pharmacodynamic * cross tolerance with benzos and barbs
71
is overdose of barbs the same cause of death as alcohol?
yes
72
what are characteristics of fetal alcohol syndrome?
* low birth weight * low brain weight * craniofacial malformation * neurological issues
73
how much greater is the risk of alcoholism if you are a relative of an alcoholic?
3-7x
74
why did benzos replace barbs?
benzos have low addiction potential and zero overdose risk
75
what positively and negatively modulates GABAa receptor?
positive: benzos negatively: B-carbolines (found in ayahuasca)
76
what affects variance in duration of different benzos?
depot binding and whether metabolites are active or inactive
77
what kind of receptor is GABAa?
ionotropic allows influx of Cl-
78
what are pharmacotherapy alcohol treatment option?
* ALDHD inhibitors * mu opioid receptor antagonist * partial NDMA antagonist
79
what benzo is used as a date rate drug?
Rohypnol
80
why are benzos used to treat chronic alcohol withdrawl?
cross-dependence
81
what kind of amnesia do benzos cause?
anterograde
82
what is the current medical use for GHB?
narcolepsy/ cataplexy

Psych 336: Drug Neuro (2 decks)

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