Havoundjian H, Paul S M, Skolnick P
Brain Res. 1986 Jun 11;375(2):401-6. doi: 10.1016/0006-8993(86)90767-5.
Rapid changes in the chloride ionophore component of the benzodiazepine-GABA receptor complex were observed in cerebral cortical membranes from rats exposed to a brief, ambient temperature swim stress. These changes were manifest as: an increase in both the efficacy and potency of chloride ions to enhance [3H]flunitrazepam binding, and an increase in both the number of [35S]t-butylbicyclophosphorothionate (a ligand that binds at or near the GABAA receptor-gated chloride ionophore) binding sites and the apparent affinity of this radioligand. These studies demonstrate that the GABA-gated, benzodiazepine-coupled chloride ionophore, which can be considered the effector component of this 'supramolecular complex', is rapidly modulated by acute stress. Such changes could represent the compensatory response of an organism to stressful or anxiety provoking changes in the environment.
在暴露于短暂环境温度游泳应激的大鼠大脑皮质膜中,观察到苯二氮䓬 - GABA受体复合物的氯离子载体成分发生了快速变化。这些变化表现为:氯离子增强[3H]氟硝西泮结合的效力和亲和力均增加,以及[35S]叔丁基双环磷硫代酸盐(一种在GABAA受体门控氯离子载体处或附近结合的配体)结合位点数量及其表观亲和力均增加。这些研究表明,可被视为这种“超分子复合物”效应成分的GABA门控、苯二氮䓬偶联的氯离子载体,会受到急性应激的快速调节。这种变化可能代表生物体对环境中应激或引发焦虑变化的代偿反应。