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急性给予戊巴比妥对大鼠脑突触神经小体中GABAA受体调节的氯离子摄取的影响。

Effects of acute pentobarbital administration on GABAA receptor-regulated chloride uptake in rat brain synaptoneurosomes.

作者信息

Yu S, Ho I K

机构信息

Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson 39216.

出版信息

Brain Res Bull. 1992 May;28(5):703-8. doi: 10.1016/0361-9230(92)90249-w.

Abstract

Effects of acute pentobarbital administration on GABAA receptor-regulated muscimol-stimulated, pentobarbital-stimulated, or flunitrazepam-enhanced, muscimol-stimulated chloride uptake were studied in the brains of Sprague-Dawley rats. Animals received sodium pentobarbital, 60 mg/kg IP, and cerebral cortical and cerebellar synaptoneurosomes were isolated at 10 min, 1 h, and when animals had awakened. The basal uptake of chloride was not changed in either cerebral cortex or cerebellum at different time periods after pentobarbital administration. Ten minutes after sodium pentobarbital administration, muscimol-stimulated chloride uptake was significantly reduced in cerebellum when the muscimol concentration was 2.5, 5, or 20 microM and in cerebral cortex when the concentration of muscimol was 5 or 10 microM (p less than 0.05, Duncan multiple-range test). One hour after pentobarbital administration or after animals had awakened, chloride uptake in brains from pentobarbital-treated animals was less at low concentration of muscimol (2.5 microM). No significant difference was found in either cerebral cortex or cerebellum in pentobarbital-(125-1,000 microM) stimulated or flunitrazepam-(2.5-20 microM) enhanced, muscimol-(3 microM) stimulated chloride uptake at different time periods after pentobarbital administration. Saline treatment had no effects on the basal or muscimol-stimulated chloride uptake in cerebellar synaptoneurosomes when compared with naive animals. The results demonstrate that GABAA receptor-regulated chloride uptake is decreased after acute pentobarbital administration, an effect that is reversible.

摘要

研究了急性给予戊巴比妥对Sprague-Dawley大鼠脑中GABAA受体调节的、由蝇蕈醇刺激的、戊巴比妥刺激的或氟硝西泮增强的、蝇蕈醇刺激的氯离子摄取的影响。动物腹腔注射60mg/kg戊巴比妥钠,在10分钟、1小时以及动物苏醒时分离大脑皮层和小脑的突触神经小体。戊巴比妥给药后不同时间段,大脑皮层和小脑中氯离子的基础摄取均未改变。戊巴比妥钠给药10分钟后,当蝇蕈醇浓度为2.5、5或20μM时,小脑中蝇蕈醇刺激的氯离子摄取显著降低;当蝇蕈醇浓度为5或10μM时,大脑皮层中蝇蕈醇刺激的氯离子摄取显著降低(P<0.05,Duncan多重极差检验)。戊巴比妥给药1小时后或动物苏醒后,戊巴比妥处理动物大脑中低浓度蝇蕈醇(2.5μM)刺激的氯离子摄取减少。戊巴比妥给药后不同时间段,在大脑皮层或小脑中,戊巴比妥(125 - 1000μM)刺激的或氟硝西泮(2.5 - 20μM)增强的、蝇蕈醇(3μM)刺激的氯离子摄取均未发现显著差异。与未处理动物相比,生理盐水处理对小脑突触神经小体中基础的或蝇蕈醇刺激的氯离子摄取没有影响。结果表明,急性给予戊巴比妥后,GABAA受体调节的氯离子摄取减少,且这种作用是可逆的。

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