作者: Natacha Vanattou-Saïfoudine , Anna Gossen , Andrew Harkin , Neuropsychopharmacology Research Group
DOI: 10.1016/J.EJPHAR.2010.10.012
关键词:
摘要: Co-administration of caffeine profoundly enhances the acute toxicity 3,4 methylenedioxymethamphetamine (MDMA) in rats. The aim this study was to determine ability impact upon MDMA-induced dopamine release superfused brain tissue slices as a contributing factor drug interaction. MDMA (100 and 300 μM) induced dose-dependent increase striatal hypothalamic preloaded with [3H] (1 μM). Caffeine also striatum hypothalamus, albeit much lesser extent than MDMA. When were (30 combination μM), enhanced release, provoking greater response that obtained following either or applications alone. synergistic effects not observed slices. As adenosine A1 receptors are, one main pharmacological targets caffeine, which are known play an important role regulation their modulation investigated. 1 μM 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), specific antagonist, like from while 2,chloro-N(6)-cyclopentyladenosine (CCPA), selective receptor agonist, attenuated this. Treatment SCH 58261, A2A rolipram, PDE-4 inhibitor, failed reproduce caffeine-like effect on release. These results suggest regulates slices, via inhibition receptors.