@article {Pierce3254, author = {R. Christopher Pierce and Peter W. Kalivas}, title = {Repeated Cocaine Modifies the Mechanism by which Amphetamine Releases Dopamine}, volume = {17}, number = {9}, pages = {3254--3261}, year = {1997}, doi = {10.1523/JNEUROSCI.17-09-03254.1997}, publisher = {Society for Neuroscience}, abstract = {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.}, issn = {0270-6474}, URL = {https://www.jneurosci.org/content/17/9/3254}, eprint = {https://www.jneurosci.org/content/17/9/3254.full.pdf}, journal = {Journal of Neuroscience} }