Journal
EUROPEAN NEUROPSYCHOPHARMACOLOGY
Volume 19, Issue 4, Pages 238-249Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.euroneuro.2008.09.004
Keywords
Methadone; Cocaine; Mu-opioid receptor; Hypocretin/orexin; Dopamine receptor
Funding
- Natural Sciences and Engineering Research Council of Canada (NSERC
- FL)
- Canadian Institutes of Health Research [79919]
- Canada Foundation for Innovation (CFI
- FL)
- Ontario Innovation Trust (OIT, FL)
- NIDA Center [P60-DA-05130]
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To elucidate the effects of steady-state methadone exposure on responding to cocaine conditioned stimuli and on cocaine-induced alterations in central opioid, hypocretin/orexin, and D2 receptor systems, mate Sprague-Dawley rats received intravenous infusions of 1 mg/kg/inf cocaine paired with an audiovisual stimulus over three days of conditioning. Then, mini pumps releasing vehicle or 30 mg/kg/day methadone were implanted (SC), and lever pressing for the stimulus was assessed in the absence of cocaine and after a cocaine prime (20 mg/kg, IP). It was found that rats treated with vehicle, but not methadone, responded for the cocaine conditioned stimulus and displayed elevated mu-opioid receptor mRNA expression in the nucleus accumbens core and basolateral amygdala, reduced hypocretin/orexin mRNA in the lateral hypothalamus, and reduced D2 receptor mRNA in the caudate-putamen. This is the first demonstration that steady-state methadone administered after cocaine exposure blocks cocaine-induced behavioral and neural adaptations. (c) 2008 Elsevier B.V. and ECNP. All rights reserved.
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