Journal
PSYCHOPHARMACOLOGY
Volume 197, Issue 3, Pages 443-448Publisher
SPRINGER
DOI: 10.1007/s00213-007-1053-z
Keywords
cocaine; morphine; motor activity; conditioned place preference; reward; beta-endorphin; proopiomelanocortin; knockout mouse
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Funding
- NIDA NIH HHS [R24 DA017298-01S1, R24 DA017298-01, R24 DA017298, R24 DA017298-02S2, DA 016682-03, R01 DA016682-03, R24 DA017298-02S1, R24 DA 017298-02, R01 DA016682, R24 DA017298-02S3, R24 DA017298-02] Funding Source: Medline
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Rationale Opioid receptor antagonists have been shown to attenuate the rewarding and addictive effects of cocaine. Furthermore, cocaine has been shown to cause the release of beta-endorphin, an endogenous opioid peptide. Objective We assessed whether this neuropeptide would play a functional role in cocaine-induced motor stimulation and conditioned place preference (CPP). Materials and methods Mice lacking beta-endorphin and their wild-type littermates were habituated to motor activity chambers for 1 h, then injected with cocaine (0, 15, 30, or 60 mg/kg, intraperitoneally) or morphine (0, 5, or 10 mg/kg, subcutaneously), and motor activity was recorded for 1 h. In the CPP paradigm, mice were tested for baseline place preference on day 1. On days 2 and 3, mice received an alternate-day saline/cocaine (15, 30, or 60 mg/kg) or saline/morphine (10 mg/kg) conditioning session and then tested for postconditioning place preference on day 4. Results Cocaine-induced motor stimulation and CPP were both reduced in mice lacking beta-endorphin. On the other hand, motor stimulation and CPP induced by morphine were not altered in mutant mice. Conclusion The present results demonstrate that the endogenous opioid peptide beta-endorphin plays a modulatory role in the motor stimulatory and rewarding actions of acute cocaine.
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