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急性应激诱导的苯二氮卓/γ-氨基丁酸受体复合物变化局限于氯离子载体。

Acute, stress-induced changes in the benzodiazepine/gamma-aminobutyric acid receptor complex are confined to the chloride ionophore.

作者信息

Havoundjian H, Paul S M, Skolnick P

出版信息

J Pharmacol Exp Ther. 1986 Jun;237(3):787-93.

PMID:3012069
Abstract

Rapid and robust changes in the chloride ionophore component of the benzodiazepine/gamma-aminobutyric acid receptor complex ("supramolecular complex") were observed in the central nervous system of rats exposed to a brief, ambient temperature swim stress. Stress-induced modification of the chloride ionophore was manifest as an increase in the efficacy of halides (Cl-, Br- and I-) to enhance [3H]flunitrazepam binding. In contrast, neither gamma-aminobutyric acid-enhanced [3H]flunitrazepam binding nor [3H] flunitrazepam binding assayed in the absence of halide ions was altered by stress. Furthermore, the number of [35S]t-butylbicyclophosphorothionate binding sites and the apparent affinity of this radioligand were increased as a result of stress, as was the ability of Cl- and low concentrations of muscimol to increase the binding of this radioligand. These changes could represent the physiological attempt of an organism to compensate for stressful changes in the environment.

摘要

在暴露于短暂环境温度游泳应激的大鼠中枢神经系统中,观察到苯二氮卓/γ-氨基丁酸受体复合物(“超分子复合物”)的氯离子载体成分发生了快速而显著的变化。应激诱导的氯离子载体修饰表现为卤化物(Cl-、Br-和I-)增强[3H]氟硝西泮结合效力的增加。相比之下,应激既未改变γ-氨基丁酸增强的[3H]氟硝西泮结合,也未改变在无卤离子情况下测定的[3H]氟硝西泮结合。此外,应激导致[35S]叔丁基双环磷硫代酸盐结合位点数量及其对该放射性配体的表观亲和力增加,Cl-和低浓度蝇蕈醇增加该放射性配体结合的能力也增加。这些变化可能代表生物体为补偿环境中的应激变化而进行的生理尝试。

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