竞争性N-甲基-D-天冬氨酸（NMDA）拮抗剂可增强δ9-四氢大麻酚在小鼠中诱导的僵住症。

Competitive NMDA antagonists enhance the catalepsy induced by delta 9-tetrahydrocannabinol in mice.

作者信息

Kinoshita H, Hasegawa T, Kameyama T, Yamamoto I, Nabeshima T

机构信息

Department of Neuropsychopharmacology, Nagoya University School of Medicine, Japan.

出版信息

Neurosci Lett. 1994 Jun 6;174(1):101-4. doi: 10.1016/0304-3940(94)90129-5.

DOI:10.1016/0304-3940(94)90129-5

PMID:7970141

Abstract

Competitive N-methyl-D-aspartate (NMDA) receptor antagonists, such as CPP and AP-7, dose-dependently enhanced the catalepsy induced by delta 9-tetrahydrocannabinol (THC; 5 mg/kg) in mice, but CPP failed to enhance haloperidol-induced catalepsy. The enhancing effect of CPP on THC-induced catalepsy was dose-dependently blocked by a muscarinic receptor antagonist, scopolamine, and by dopamine D1 and D2 receptor agonists such as apomorphine, SKF 38393 and quinpirole. The effect of CPP was quite opposite to that of the noncompetitive NMDA receptor antagonist MK-801. Therefore, the THC-induced catalepsy model may be useful for distinguishing between both classes of NMDA receptor antagonists.

摘要

竞争性N-甲基-D-天冬氨酸（NMDA）受体拮抗剂，如CPP和AP-7，可剂量依赖性地增强δ9-四氢大麻酚（THC；5毫克/千克）诱导的小鼠僵住症，但CPP未能增强氟哌啶醇诱导的僵住症。CPP对THC诱导的僵住症的增强作用可被毒蕈碱受体拮抗剂东莨菪碱以及多巴胺D1和D2受体激动剂如阿扑吗啡、SKF 38393和喹吡罗剂量依赖性地阻断。CPP的作用与非竞争性NMDA受体拮抗剂MK-801的作用完全相反。因此，THC诱导的僵住症模型可能有助于区分这两类NMDA受体拮抗剂。