Cocaine-conditioned place preference by dopamine-deficient mice is mediated by serotonin.
paper
Cited
Public
Unavailable
- Authors
- Hnasko, Thomas S; Sotak, Bethany N; Palmiter, Richard D
- Year
- 2007
- Journal
- The Journal of neuroscience : the official journal of the Society for Neuroscience
- PMID
- 18003826
- DOI
- 10.1523/JNEUROSCI.3133-07.2007
- PMCID
- PMC6673324
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 D1-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 D2-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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