Miller L G, Thompson M L, Greenblatt D J, Deutsch S I, Shader R I, Paul S M
Brain Res. 1987 Jun 30;414(2):395-400. doi: 10.1016/0006-8993(87)90023-0.
Defeat stress in mice, a model of social stress, increases benzodiazepine receptor binding as measured by specific [3H]Ro15-1788 binding in vivo, but not by [3H]flunitrazepam binding in vitro. This increase occurs rapidly, by 20 min following exposure to stress, and resolves by 60 min. Increased benzodiazepine receptor binding is observed in the cerebral cortex, cerebellum and hypothalamus, and appears to be due to an increase in receptor number rather than apparent affinity. The stress-induced increase in central benzodiazepine receptors is decreased in a dose-dependent fashion by lorazepam, a benzodiazepine agonist, but not by the receptor antagonist Ro15-1788. The stress-induced increase in benzodiazepine receptors is also blocked by adrenalectomy and is restored by corticosterone replacement.
在小鼠（一种社会应激模型）中克服应激，会增加体内通过特异性[3H]Ro15 - 1788结合所测量的苯二氮䓬受体结合，但体外[3H]氟硝西泮结合则无此现象。这种增加迅速发生，在暴露于应激后20分钟时出现，并在60分钟时恢复。在大脑皮层、小脑和下丘脑观察到苯二氮䓬受体结合增加，这似乎是由于受体数量增加而非表观亲和力增加所致。苯二氮䓬激动剂劳拉西泮以剂量依赖方式降低应激诱导的中枢苯二氮䓬受体增加，但受体拮抗剂Ro15 - 1788则无此作用。应激诱导的苯二氮䓬受体增加也被肾上腺切除术阻断，并通过皮质酮替代得以恢复。
