The Journal of Neuroscience, 2001, 21:RC184:1-5
RAPID COMMUNICATION
Stimulation of Endorphin Neurotransmission in the Nucleus
Accumbens by Ethanol, Cocaine, and Amphetamine
M. Foster
Olive1,
Heather N.
Koenig1,
Michelle A.
Nannini1, and
Clyde W.
Hodge2
1 Department of Neurology and Ernest Gallo Clinic and
Research Center, University of California at San Francisco,
Emeryville, California 94608, and 2 Center for Alcohol
Studies, School of Medicine, University of North Carolina at Chapel
Hill, Chapel Hill, North Carolina 27599
Numerous studies have demonstrated that drugs of abuse activate the
mesolimbic dopamine reward pathway, and it is widely held that this
activation contributes to the motivational and positive reinforcing
properties of these substances. However, there is evidence that
endogenous opioid systems within this brain reward circuit also play a
role in drug reinforcement and drug-seeking behavior. Using
microdialysis in freely moving rats, we sought to determine whether
various drugs of abuse (i.e., ethanol, cocaine, D-amphetamine, and nicotine) would increase
neurotransmission of endogenous opioid peptides (i.e., endorphins) in
the nucleus accumbens. Drugs were administered intraperitoneally twice
at 3 h intervals, and the endorphin content of microdialysates was analyzed by a solid-phase radioimmunoassay. Acute administration of
ethanol, cocaine, and D-amphetamine transiently elevated
extracellular levels of endorphins in the nucleus accumbens, whereas
nicotine and saline were without effect. We hypothesize that this
drug-induced release of endorphins may contribute to the positive
reinforcing and motivating properties of ethanol and psychostimulants.
Key words:
microdialysis; endorphin; cocaine; ethanol; amphetamine; nicotine; addiction
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