Fomenko A I, Donchenko G V, Khalmuradov A A, Stepanenko S P
Ukr Biokhim Zh (1978). 1997 Mar-Apr;69(2):46-50.
Nitrozepam has been shown to decrease specific binding of [14C]NAD by the synaptic mem-branes approximately by 40%. Alongside with the latter GABA in the concentration of 10(-5) M potentiates the effect observed. Blocking in vitro of GABA receptors by bicuculin removes both the tranquilizer and GABA effect. While simulating epileptogenesis in animals the nitrazepam effect on [14C]NAD specific binding sites was somewhat more expressed in comparison with the norm. The interaction of NAD reception systems with benzodiazepine under the pathology is capable to be mediated not only by increasing GABA-ergic transfer, but it can occur place without GABA-ergic component of GABA-benzodiazepine receptor complex.
已证明硝西泮可使突触膜对[14C]NAD的特异性结合减少约40%。与此同时，浓度为10(-5) M的γ-氨基丁酸（GABA）可增强所观察到的效果。在体外，荷包牡丹碱阻断GABA受体可消除镇静剂和GABA的作用。在模拟动物癫痫发生时，与正常情况相比，硝西泮对[14C]NAD特异性结合位点的作用表现得更为明显。在病理状态下，NAD受体系统与苯二氮䓬的相互作用不仅可通过增强GABA能传递来介导，而且也可能在没有GABA-苯二氮䓬受体复合物的GABA能成分参与的情况下发生。
