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基底核损伤所致空间导航缺陷被苯二氮䓬受体拮抗剂ZK 93 426减弱。

Attenuation by the benzodiazepine receptor antagonist, ZK 93 426, of the deficit in spatial navigation induced by nucleus basalis lesions.

作者信息

Mazurkiewicz M, Sirviö J, Riekkinen P

机构信息

Department of Neurology, University of Kuopio, Finland.

出版信息

Behav Neural Biol. 1992 Sep;58(2):159-63. doi: 10.1016/0163-1047(92)90411-v.

Abstract

The effects of the benzodiazepine receptor antagonist, beta-carboline ZK 93,426 treatment were studied both in NB-lesioned (ibotenic acid) and in unoperated Kuo-Wistar rats in a water maze task. The ZK 93,426 administered in the doses of 1 and 5 mg/kg, 30 min prior to the testing in a water maze apparatus, attenuated the NB lesion-induced spatial navigation deficit, although it had no effect on the performance of unoperated rats. The results suggest functional interactions between GABAergic system and ibotenic acid-induced lesion of the basal forebrain in rats.

摘要

在水迷宫任务中,研究了苯二氮䓬受体拮抗剂β-咔啉ZK 93,426对经鹅膏蕈氨酸损伤(鹅膏蕈氨酸)的大鼠和未手术的阔耳-威斯塔大鼠的治疗效果。在水迷宫装置中测试前30分钟,以1和5毫克/千克的剂量给予ZK 93,426,减轻了鹅膏蕈氨酸损伤诱导的空间导航缺陷,尽管它对未手术大鼠的表现没有影响。结果表明大鼠中γ-氨基丁酸能系统与鹅膏蕈氨酸诱导的基底前脑损伤之间存在功能相互作用。

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