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Intravenous administration of the cannabinoid CB₁ receptor agonists (R-(+)-[2,3-Dihydro-5-methyl-3[morpholinyl)methyl]-pyrrolo[1,2,3-de]-1,4-benzoxazinyl]-(1-naphthalenyl)methanone mesylate), WIN 55,212-2 (10, 37.5, 75 and 150 μg/kg), and ((6aR)-trans-3-(1,1-Dimethylheptyl)-6a,7,10,10a-tetrahydro-1-hydroxy-6,6-dimethyl-6H-dibenzo[b,d]pyran-9-methanol), HU 210 (1 and 4 μg/kg) dose-dependently increased acetylcholine release in dialysates from the prefrontal cortex and the hippocampus of freely moving rats. Administration of the cannabinoid receptor antagonist {N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3carboxamide}HCl, SR 141716A, at a dose that per se did not affect basal acetylcholine release (2.5 μg/kg), prevented the increase of acetylcholine release by WIN 55,212-2 (150 μg/kg i.v.) or by HU 210 (4 μg/kg i.v.) in both areas. These data demonstrate that, at …