These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Dopaminergic mechanism for caffeine-produced cocaine seeking in rats.
    Author: Green TA, Schenk S.
    Journal: Neuropsychopharmacology; 2002 Apr; 26(4):422-30. PubMed ID: 11927167.
    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.
    [Abstract] [Full Text] [Related] [New Search]