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PK 8165的行为效应并非由苯二氮䓬结合位点介导。

Behavioural effects of PK 8165 that are not mediated by benzodiazepine binding sites.

作者信息

File S E, Pellow S

出版信息

Neurosci Lett. 1984 Sep 7;50(1-3):197-201. doi: 10.1016/0304-3940(84)90486-5.

Abstract

The phenylquinoline, PK 8165 (5-25 mg/kg), produced dose-related reductions in locomotor activity, rearing and exploratory head-dipping in a holeboard. Neither Ro 15-1788 (1, 10 or 20 mg/kg) nor CGS 8216 (1 or 10 mg/kg) was able to reverse the reductions in locomotor activity or rearing. This suggests that at least some of the behavioural effects of PK 8165 are not mediated by a site on the GABA-benzodiazepine receptor complex. This conclusion is supported by the recent report [9] that, whereas PK 8165 potently displaces benzodiazepines from their binding site in vitro, it is without effect in vivo.

摘要

苯基喹啉PK 8165(5 - 25毫克/千克)可使自发活动、竖毛行为及在洞板实验中的探究性探首行为呈剂量依赖性减少。Ro 15 - 1788(1、10或20毫克/千克)及CGS 8216(1或10毫克/千克)均无法逆转自发活动或竖毛行为的减少。这表明PK 8165的至少某些行为效应并非由GABA - 苯二氮䓬受体复合物上的位点介导。近期报告[9]支持了这一结论,即尽管PK 8165在体外能有效地将苯二氮䓬从其结合位点置换下来,但在体内却无此作用。

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