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Volume 17, Number 9, Issue of May 1, 1997 pp. 3254-3261
Copyright ©1997 Society for NeuroscienceRepeated Cocaine Modifies the Mechanism by which Amphetamine Releases Dopamine
Received Oct. 28, 1996; revised Feb. 3, 1997; accepted Feb. 6, 1997.
R. Christopher Pierce and Peter W. Kalivas Alcohol and Drug Abuse Program, Washington State University, Pullman, Washington 99164-6520
This study determined whether daily cocaine administration initiates a calcium requirement for the increase in extracellular dopamine produced by psychostimulants. The increase in extracellular dopamine induced by perfusion of amphetamine through a microdialysis probe in the nucleus accumbens shell was enhanced in cocaine- relative to saline-pretreated rats. The augmented portion of the amphetamine-induced increase in nucleus accumbens dopamine was abolished by the coperfusion of L- or N-type calcium channel blockers. Inhibition of calcium/calmodulin-dependent protein kinase II (CaM-KII) also prevented the augmented increase in dopamine by amphetamine, whereas inhibition of vesicular exocytosis by botulinum toxin B was ineffective. When the concentration of extracellular dopamine in the nucleus accumbens was elevated by blocking the plasmallemal dopamine transporter with GBR-12909, the augmented increase in extracellular dopamine in rats sensitized to repeated cocaine was blocked by a CaM-KII inhibitor. Pretreatment with botulinum toxin B prevented the increase in extracellular dopamine by GBR-12909 in both cocaine-pretreated and control rats. Taken together, these results demonstrate that the psychostimulant-induced enhanced increase in extracellular dopamine in the nucleus accumbens shell of cocaine-pretreated rats arises from the induction of calcium- and CaM-KII-dependent mechanisms.
Key words: behavioral sensitization; cocaine; amphetamine; GBR-12909; verapamil; conotoxin; diltiazem; KN-93; botulinum toxin; calcium; calmodulin
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