Kinoshita H, Hasegawa T, Katsumata Y, Kameyama T, Yamamoto I, Nabeshima T
Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine, Japan.
J Neural Transm Gen Sect. 1994;95(2):137-43. doi: 10.1007/BF01276432.
Mice treated with delta 9-tetrahydrocannabinol (THC; 5 and 10 mg/kg i.v.) showed the catalepsy in high bar test, and median descent latencies of catalepsy were about 150 sec. Dizocilpine (MK-801, 0.05 and 0.1 mg/kg), non-competitive N-methyl-D-aspartate (NMDA) antagonist, significantly attenuated THC-induced catalepsy. Furthermore, the anticataleptic effect of MK-801 on THC-induced catalepsy was blocked by acetylcholine agonist oxotremorine (0.005 mg/kg) and dopamine antagonist haloperidol (0.01 mg/kg), but not by NMDA. Oxotremorine, haloperidol, and NMDA themselves did not affect THC-induced catalepsy at the doses used. These results suggest that the anticataleptic effect of MK-801 on THC-induced catalepsy may be developed through dopaminergic and acetylcholinergic neuronal systems.
用δ9 - 四氢大麻酚(THC;静脉注射5毫克/千克和10毫克/千克)处理的小鼠在高架试验中出现僵住症,僵住症的中位下降潜伏期约为150秒。非竞争性N - 甲基 - D - 天冬氨酸(NMDA)拮抗剂地佐环平(MK - 801,0.05毫克/千克和0.1毫克/千克)显著减轻了THC诱导的僵住症。此外,MK - 801对THC诱导的僵住症的抗僵住作用被乙酰胆碱激动剂氧化震颤素(0.005毫克/千克)和多巴胺拮抗剂氟哌啶醇(0.01毫克/千克)阻断,但未被NMDA阻断。氧化震颤素、氟哌啶醇和NMDA本身在所使用的剂量下不影响THC诱导的僵住症。这些结果表明,MK - 801对THC诱导的僵住症的抗僵住作用可能是通过多巴胺能和乙酰胆碱能神经系统产生的。