Acquas E, Pisanu A, Marrocu P, Di Chiara G
Department of Toxicology, University of Cagliari and Centre for Neuropharmacology, CNR, V.le A. Diaz, 182, 09126, Cagliari, Italy.
Eur J Pharmacol. 2000 Aug 4;401(2):179-85. doi: 10.1016/s0014-2999(00)00403-9.
Intravenous administration of the cannabinoid CB(1) 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 microg/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 microg/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-3 carboxamide]HCl, SR 141716A, at a dose that per se did not affect basal acetylcholine release (2. 5 microg/kg), prevented the increase of acetylcholine release by WIN 55,212-2 (150 microg/kg i.v.) or by HU 210 (4 microg/kg i.v.) in both areas. These data demonstrate that, at low i.v. doses, the synthetic cannabinoid CB(1) receptor agonists, WIN 55,212-2 and HU 210 stimulate cortical and hippocampal acetylcholine release.
静脉注射大麻素CB(1)受体激动剂（R-(+)-[2, 3-二氢-5-甲基-3-[吗啉基)甲基]-吡咯并[1,2,3-de]-1, 4-苯并恶嗪基]-(1-萘基)甲酮甲磺酸盐），WIN 55,212-2（10、37.5、75和150微克/千克），以及((6aR)-反式-3-(1, 1-二甲基庚基)-6a,7,10,10a-四氢-1-羟基-6, 6-二甲基-6H-二苯并[b,d]吡喃-9-甲醇），HU 210（1和4微克/千克），可剂量依赖性地增加自由活动大鼠前额叶皮质和海马区透析液中乙酰胆碱的释放。以本身不影响基础乙酰胆碱释放的剂量（2.5微克/千克）给予大麻素受体拮抗剂[N-(哌啶-1-基)-5-(4-氯苯基)-1-(2, 4-二氯苯基)-4-甲基-1H-吡唑-3-甲酰胺]HCl，SR 141716A，可阻止WIN 55,212-2（150微克/千克静脉注射）或HU 210（4微克/千克静脉注射）在这两个区域引起的乙酰胆碱释放增加。这些数据表明，在低静脉注射剂量下，合成大麻素CB(1)受体激动剂WIN 55,212-2和HU 210可刺激皮质和海马区乙酰胆碱的释放。
