Corda M G, Concas A, Biggio G
Neurosci Lett. 1985 May 23;56(3):265-9. doi: 10.1016/0304-3940(85)90253-8.
The cerebral cortex of unstressed rats has a higher density of low affinity gamma-aminobutyric acid (GABA) receptors than that of stressed animals. Stress (handling or foot shock) produces a sudden decrease in the total number of low-affinity GABA receptors in the cerebral cortex of unstressed rats but leaves unchanged the density of GABA receptors in the cortex of stressed animals. The in vivo administration of Ro 15-1788 (30 mg/kg per os), a specific benzodiazepine receptor antagonist, completely prevents the effect of footshock on the low-affinity GABA receptors. The results suggest that (a) benzodiazepine recognition sites are involved in the action of stress on GABA receptors, and (b) stress may release an endogenous ligand for the benzodiazepine recognition site.
未受应激的大鼠大脑皮层中低亲和力γ-氨基丁酸（GABA）受体的密度高于受应激动物。应激（处理或足部电击）会使未受应激大鼠大脑皮层中低亲和力GABA受体的总数突然减少，但对应激动物皮层中GABA受体的密度没有影响。特异性苯二氮䓬受体拮抗剂Ro 15-1788（30毫克/千克口服）的体内给药完全阻止了足部电击对低亲和力GABA受体的影响。结果表明：（a）苯二氮䓬识别位点参与了应激对GABA受体的作用；（b）应激可能释放出一种苯二氮䓬识别位点的内源性配体。
