lecture 17 LOs Flashcards
in ‘drinker’ rats, what makes them this way
the dopamine system is much more responsive to alcohol than their counterpart non drinkers
endogenous opioids contribute to reinforcing effects of alcohol, how
- acute alcohol increases endorphin and enkephalin production or release
- alcohol-induced opioid release may contribute to its ability to increase DA release
- chronic alcohol reduces opioid production which may contribute to he dysphoria that accompanies chronic alcohol use and withdrawal
what do opioid receptor antagonists do to alcohol self administration
it reduces it
what happens to mu opioid receptor knockout mice
they fail to self administer ethanol
what is the mechanism of action for nicotine
acts as a direct agonist to active nicotinic cholinergic receptors
(excitatory effects on neural activity)
what does nicotine do to non smokers
aversive effects, elicits heightened tension/arousal, lightheadedness, dizziness, nausea
what does nicotine do to smokers
mild arousal (stimulant effect), calm or relaxed state (relief from withdrawal symptoms), appetite suppression
what cog effects can nicotine have on attention
enhancing effects
what NT plays a role in nicotine reinforcement
mesolimbic DA
where do nicotine receptors reside
DA neurons cell bodies (to stimulate firing and increase NAc DA release)
where does nicotine heteroreceptors reside
also on DA terminals in NAc (to increase transmitter release)
what lesions attenuate nicotine self administration
DA terminals in NAc
regarding nicotine, what happens when DA receptors are blocked
disrupts conditioned place preference to nicotine (measure of drug reward) and reinstatement of nicotine seeking, suggesting DA contributes to relapse
what is a genetic way to prevent nicotine self administration
genetic knockout of certain nicotine receptor subtypes
what are two examples of conditioned reinforcers for nicotine
sensory and temporal stimuli associated with the act of smoking become conditioned to reinforcing effects