primary mechanism of reinforcement; cell bodies in VTA, projects to NAc and AMY; brain stimulation, natural rewards
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mesocortical system
secondary mechanism; DA cell bodies in the VTA, projects to PFC
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endorphins
morphine-like NTs found in the brain and pituitary gland
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incentive sensitization hypothesis
sensitization of mesocorticolimbic DA systems; increased sensitivity to stimulus; stimuli is more valuable because the system has been conditioned to it
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tolerance
the need to take increasingly higher doses of a drug to achieve a particular effect
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withdrawal
when cessation of drug use elicits symptoms opposite to those produced by the drug [negative reinforcement]
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hallucinogens
5-HT2A agonists
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serotonin-like hallucinogens
same group as LSD, psilocybin, DMT
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catecholamine-like hallucinogens
same group as mescaline (Peyote), DOM
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LSD
psychological effects 30-90 minutes after oral administration; peak effect at 2-4 hours; strange sensory experiences even after taking it regularly, quick tolerance
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hallucinogen persisting perception disorder
individuals have flashbacks, sensory experiences, years after cessation of use
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THC (marijuana)
indirect glutamate antagonist
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THC mechanism of action
binds to cannabinoid receptors; CBR are GPCRs which inhibit Ca2+ influx; partial agonist on CBR, antagonist at Glu terminals
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anandamide
partial agonist of the CBR, endogenous ligand for the CBR
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THC
injections of these result in an increase in DA in the NAcd
binds to GABA-A receptor, increases DA in the NAc, addictive
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mechanism of action of alcohol
binds to allosteric GABA-A receptor (BZD site), increases DA in NAc
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Korsakoff's Syndrome
lack of B1 which causes dmg in the limbic system and cortexa
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anterograde amnesia
inability to form new memories
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retrograde amnesia
severe loss of memories formed before the onset of the condition
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confabulation
invented memories which are then taken as true due to gaps in memory sometimes associated with blackout
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cocaine, amphetamines
DA-based stimulants
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caffeine
mild reinforcement, binds to adenosine receptors in the brain, addiction leads to mildly unpleasant withdrawal effects
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nicotine mechanism of action
acts on ACh nicotinic receptors; DA in NAc (reinforcement), tendency to relapse
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amphetamines mechanism of action
causes DA to come out of vesicles intraneuronally, causes DA reuptake TP to run in reverse, flooding synapses with DA
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Ritalin
blocks DA reuptake; weaker affinity to DAT
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MDMA
serotonergic drug of abuse
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MDMA mechanism of action
causes DA, NE, and 5HT to come out of vesicles intraneuronally; reuptake TP runs in reverse, flooding synapses, binds to 5HT receptors
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spinothalamic tract
cell bodies in DRG; synapses and crosses into spinal cord, ascends in the lateral horn; axons in the medial lemniscus; projects to VPN of the thalamus which projects to S1
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A-delta fibers
lightly myelinated and smaller diameter; used for rapid, sharp pain, initial reflex response
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C fibers
unmyelinated and smallest fibers; used for slow, burning pain
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spinoreticular
axons ascend to brainstem reticular formation (arousal/responding), projects to VPN, hypothalamus, cortex; used for emotional aspects of pain
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descending inhibitory pain modulation
PAG in the midbrain and RVM; projects to dorsal horn of spinal cord which inhibits pain transmission
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enkpehalins
morphine-like NTs found in the brain and adrenals
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descending pain control pathway
DLPF activates ACC system which activates PAG, raphe nuclei, travels to dorsolateral funiculus of spinal cord, synapses on inhibitory interneurons in dorsal horn of spinal cord which release endogenous opioids
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opium
raw latex fr poppy
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opiates
compounds purified from opium poppy.
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opioids
any molecule exhibiting the properties, natural or synthetic
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opioid peptides
endogenously produced peptide molecules that activate opioid receptors