Author(s): Green TA, Schenk S
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Abstract Systemic administration of caffeine reinstates extinguished cocaine self-administration behavior in rats, but the mechanism mediating this behavioral effect has not been established. The present study examined the role of adenosinergic A2 and dopaminergic mechanisms in caffeine-produced cocaine seeking. Following extinction of cocaine self-administration, experimenter-administered injections of caffeine (1.25-20 mg/kg) and theophylline (1-10 mg/kg) dose-dependently reinstated extinguished cocaine-seeking behavior. Administration of the adenosinergic A2 antagonist, 3,7-dimethyl-1-propargylxanthine (DMPX; 0.546-2.18 microg/kg), failed to produce cocaine seeking. Pretreatment with doses of the adenosine A1/A2 agonist 5'-N-ethylcarboxamidoadenosine (NECA; 0.003-0.03 mg/kg) that were below those that produced marked sedation failed to block reinstatement. These data suggest that methylxanthine-produced cocaine seeking is not due to adenosine A2 receptor antagonism. In contrast, pretreatment with the dopaminergic D1-like antagonist SCH 23390 (0.005-0.02 mg/kg) or the D2-like antagonist eticlopride (0.03-0.3 mg/kg) produced a dose-dependent attenuation of caffeine-produced reinstatement at doses that did not decrease cocaine self-administration. These findings suggest that dopaminergic mechanisms underlie the ability of caffeine to reinstate extinguished cocaine-taking behavior.
This article was published in Neuropsychopharmacology
and referenced in Journal of Addiction Research & Therapy