Journal
JOURNAL OF NEUROSCIENCE
Volume 27, Issue 46, Pages 12484-12488Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3133-07.2007
Keywords
cocaine; conditioned place preference; dopamine; dopamine-deficient; dopamine transporter; serotonin transporter
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Funding
- NIDA NIH HHS [P50-DA13410] Funding Source: Medline
- NIGMS NIH HHS [T32 GM07270, T32 GM007270] Funding Source: Medline
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Rodents learn to associate the rewarding effects of drugs with the environment in which they are encountered and, subsequently, will display a conditioned place preference (CPP) for that environment. Cocaine-induced CPP is generally thought to be mediated through inhibition of the dopamine transporter and the consequent increase in extracellular dopamine. However, here we report that dopamine-deficient (DD) mice formed a CPP for cocaine that was not blocked by a dopamine D-1-receptor antagonist. Fluoxetine, a serotonin transporter (SERT) inhibitor, produced CPP in DD, but not control mice, suggesting that serotonin mediates cocaine CPP in DD mice. Inhibition of dopamine neuron firing by pretreatment with quinpirole, a dopamine D-2-receptor agonist, blocked both cocaine-and fluoxetine-induced CPP in DD mice. These findings are consistent with the hypothesis that, in the absence of dopamine, cocaine-mediated SERT blockade activates dopamine neurons, which then release some other neurotransmitter that contributes to cocaine reward in DD mice.
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