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PMCOL 305 > 3 - Addiction > Flashcards

3 - Addiction Flashcards

1
Q

reward circuit

A
  1. descending glutamatergic pathway from anterior bed nuclei to VTA
  2. ascending dopaminergic VTA to NAc
  3. GABA-ergic NAc pathway to ventral palllidum
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2
Q

neurotransmitters in addiction

A
  • dopamine
  • glutamate
  • GABA
  • norepinephrine
  • acetylcholine
  • serotonin
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3
Q

dopamine (DA)

A
  • catecholamine
  • primary driver of reward circuit
  • 2nd step in reward circuit
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4
Q

glutamate (Glu)

A
  • amino acid
  • major role in relapse (cue-triggering)
  • LTP/LTD plasticity (adapting)
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5
Q

GABA

A
  • inhibitory

- major role in disinhibitory mechanisms of reward (no self-control)

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6
Q
  • norepinephrine (NE)
A
  • catecholamine (NTs released in stress)

- comes from locus coeruleus in brain

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7
Q

acetylcholine (ACh)

A
  • receptors found in VTA DA-ergic neurons

- major role in learning/memory

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8
Q

serotonin (5-HT)

A
  • monoamine indole (hallucinogens)
  • comes from raphe nuclei
  • low source of 5-HT results in violence and impulse actions
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9
Q

dopamine receptors (DRs)

A
  • 5 genes
  • all GPCRs
  • D1-like type
  • D2-like type
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10
Q

D1-like type receptors

A
  • D1 and D5
  • Gs coupled
  • increase cAMP via adenylyl cyclase
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11
Q

D2-like type receptors

A
  • D2, D3, and D4
  • Gi coupled
  • decrease cAMP via adenylyl cyclase
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12
Q

role of dopamine in addiction from animal tests

A
  • effort exerted in self-administration is directly proportional to the degree of reward
  • conditioned place preference
  • nicotine injections produced CPP and voluntary self-administration
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13
Q

conditioned place preference (CPP)

A
  • the link of an environment with VTA DA-ergic projections
  • results in animal’s preference in drug related chamber
  • time spent in the drug-paired chamber = drug-seeking behaviour
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14
Q

neurotransmitter levels

A
  • measured in nuclei with microdialysis

- inputs made to the reward circuit control hedonic tone

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15
Q

dopamine antagonists

A
  • negative reinforcers
  • enhance behaviours in attempts to decrease administration of a drug
  • causes aversive effects (punish stimulus behaviour), therefore drug-taking behaviour is ceased
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16
Q

microdialysis in NAc

A
  1. first dose increases tonic extracellular level by 200%
  2. fluctuates between 100-200%
  3. low points predict next self-administered dose
17
Q

tolerance in addicts

A
  • leads to lowered hedonic tone, therefore more drug is required to mimic euphoric effect from 1st dose
  • depressed activity in the reward circuit post-use (withdrawl stages) causes dysphoria
18
Q

sensitization

A

reverse tolerance (moves further away from baseline)

19
Q

AMPA receptors (AMPARs)

A
  • 4 genes, 4 protein subunits
  • fast, excitatory transmission
  • ionotropic (membrane-bound receptor proteins)
  • forms tetramers
  • C-terminus forms intracellular scaffolds
  • major role in LTD
20
Q

N-methyl-D-aspartate receptors (NMDARs)

A
  • 7 genes, 7 protein subunits
  • ionotropic (membrane-bound receptor proteins)
  • coactivated by Glu AND Ser/Gly
  • calcium dependent
  • subunits are heterotetramer (2 GluN1 + 2GluN2)
  • major role in LTP/LTD
21
Q

glutamate receptors (mGlu-R)

A
  • 8 genes
  • metabotropic (metabolic steps for activity)
  • group C GPCRs
  • each encodes a receptor
  • involved in synaptic plasticity (change in synapses)
  • Group 1
  • Group 2/3
22
Q

Group 1 mGlu-R

A
  • Gq-linked
  • increase excitotoxicity risk
  • explains lower volume of addicts’ brains as cells are dying
23
Q

Group 2 mGlu-R

A
  • Gi/o-linked

- decrease excitotoxicity risk

24
Q

long-term potentiation (LTP)

A
  • strengthening of synaptic transmission between two neurons downstream of glutamate receptors
25
Q

activity-dependent changes effects

A

changes in neurotransmitter release can also change structure as well

26
Q

specificity of LTP

A

confined to specific contact sites

27
Q

associativity of LTP

A

strong stimulation in one pathway will induce LTP for weak pathways (pathways pushed to overdrive)

28
Q

cooperativity of LTP

A

many weak stimuli induces LTP through constructive interference

29
Q

persistance of LTP

A
  • potentiation can last min, wks, … etc.

- unique to LTP (this is not what happens in other plasticity)

30
Q

long-term depression (LTD)

A

weakening of synaptic transmission between two neurons

31
Q

dopamine prediction error hypothesis

A
  • an unexpected reward in phasic firing of VTA DA-ergic neurons resulted in learning
  • learning stops when reward is predictable, therefore DA-ergic neurons are not triggered
  • learning signal leads to drug adaptive behaviours, therefore there is a compulsive drug intake at the expense of all other behaviours
  • ex: lab animals prefer drugs over food, water, toys, sex, even if it causes pain
32
Q

NE in addiction

A
  • innervation activates sympathetic responses

- major role in stress-induced relapse

33
Q

5-HT in addiction

A
  • binds several 5-HT receptors that are triggered by hallucinogens and entactogenic drugs
  • drugs binding the receptors are less addicting
  • bi-synaptic 5-HT inputs to the VTA and NAc from RN
34
Q

ACh in addiction

A
  • activates parasympathetic responses
  • major role in learning and memory circuits
  • nicotinic ACh receptors display several isoforms with brain region-specific expression including on VTA DA-ergic neurons
35
Q

pleiotropic

A
  • all drugs are pleiotropic
  • psychoactive effects do not occur in isolation
  • long periods of addiction causes tissues to become dysfunctional
36
Q

cocaine pleiotropy

A
  • damages heart cell sarcolemmal membranes

- releases lactate dehydrogenase

37
Q

smoking pleiotropy

A
  • sustained stress

- inflammation in oral/lung tissue

38
Q

alcohol pleiotropy

A

liver disease (epicentre of dysfunction)

PMCOL 305 (8 decks)

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