Lippa A S, Critchett D, Sano M C, Klepner C A, Greenblatt E N, Coupet J, Beer B
Pharmacol Biochem Behav. 1979 May;10(5):831-43. doi: 10.1016/0091-3057(79)90342-3.
Brain specific benzodiazepine receptors appear to mediate the pharmacological properties of benzodiazepines. A neuronal localization for these receptors is suggested by the parallel decrease in the number of benzodiazepine receptors and cerebellar Purkinje cells in "nervous" mutant mice. Electrophysiological results are compatible with an action of benzodiazepines on neuronally localized, physiological receptors. Biochemical, electrophysiological and behavioral experiments highlight the possible importance of frontal cortex in mediating the anxiolytic properties of the benzodiazepines. Triazolenetetrazoles act upon benzodiazepine receptors, increase punished responding and protect against penetylenetetrazole-induced convulsions, but do not produce the side effects associated with benzodiazepines or affect classical neurotransmitter systems. The structural similarities between triazolopyridazines, purines and the indole portion of certain peptides may provide insights into the nature of the endogenous ligand.
脑特异性苯二氮䓬受体似乎介导了苯二氮䓬类药物的药理特性。“神经质”突变小鼠中苯二氮䓬受体数量与小脑浦肯野细胞数量的平行减少表明了这些受体的神经元定位。电生理结果与苯二氮䓬类药物作用于神经元定位的生理受体的观点相一致。生化、电生理和行为实验突出了额叶皮质在介导苯二氮䓬类药物抗焦虑特性方面的潜在重要性。三唑并四氮唑作用于苯二氮䓬受体,增加受惩罚反应并预防戊四氮诱导的惊厥,但不会产生与苯二氮䓬类药物相关的副作用,也不会影响经典神经递质系统。三唑并哒嗪、嘌呤与某些肽的吲哚部分之间的结构相似性可能为内源性配体的性质提供见解。