Gardner C R
Comp Biochem Physiol C Comp Pharmacol Toxicol. 1986;85(1):225-32. doi: 10.1016/0742-8413(86)90078-2.
An exponential relationship was observed between the firing rate of cerebellar Purkinje cells in urethane-anaesthetized rats and the duration of inhibition evoked in these cells by electrical stimulation of the nearby cortical surface. Benzodiazepines, administered i.v., decreased cell firing and increased the duration of the inhibitory response but did not alter the relationship between the two parameters. These effects of one benzodiazepine, RU 32007, were reversed by the benzodiazepine antagonist Ro15-1788 which had little effect alone. The benzodiazepine inverse agonists methyl- or ethyl-beta-carboline-3-carboxylate increased cell firing with the expected reductions in duration of inhibitory response in some cases. However, in 50% of recordings the inhibitory response disappeared, independent of the firing rate. All the effects of the beta-carboline esters were reversed by Ro15-1788 or the benzodiazepine, RU 32007. This action of the benzodiazepine receptor inverse agonists represents an in vivo blockade of an endogenous synaptic inhibition which is thought to be mediated by release of GABA.
在氨基甲酸乙酯麻醉的大鼠中，观察到小脑浦肯野细胞的放电频率与通过电刺激附近皮质表面在这些细胞中诱发的抑制持续时间之间呈指数关系。静脉注射苯二氮䓬类药物可降低细胞放电频率并增加抑制反应的持续时间，但不会改变这两个参数之间的关系。一种苯二氮䓬类药物RU 32007的这些作用可被苯二氮䓬类拮抗剂Ro15 - 1788逆转，而Ro15 - 1788单独作用时影响很小。苯二氮䓬类反向激动剂甲基 - 或乙基 - β - 咔啉 - 3 - 羧酸酯在某些情况下增加细胞放电频率，并预期会缩短抑制反应的持续时间。然而，在50%的记录中，抑制反应消失，与放电频率无关。Ro15 - 1788或苯二氮䓬类药物RU 32007可逆转β - 咔啉酯的所有作用。苯二氮䓬类受体反向激动剂的这种作用代表了对一种内源性突触抑制的体内阻断，这种抑制被认为是由γ - 氨基丁酸（GABA）的释放介导的。
