Barker J L, Harrison N L, Mariani A P
Life Sci. 1986 Nov 24;39(21):1959-68. doi: 10.1016/0024-3205(86)90319-x.
Many neurons cultured from the embryonic mammalian central nervous system (CNS) express benzodiazepine receptors while some neurons differentiate specific transmitter phenotypes like glutamic acid decarboxylase (GAD), the synthetic enzyme for gamma-aminobutyric acid (GABA). The benzodiazepine receptors in these cultured neurons are often, if not always coupled to a practically ubiquitous GABA-mediated function, activation of Cl- ion conductance. The transmitter signal serves to inhibit neuronal excitability and is facilitated by clinically important benzodiazepines. Here we review some details regarding the pharmacological actions of benzodiazepines on membrane excitability.
许多从胚胎哺乳动物中枢神经系统(CNS)培养的神经元表达苯二氮䓬受体,而一些神经元则分化出特定的递质表型,如谷氨酸脱羧酶(GAD),即γ-氨基丁酸(GABA)的合成酶。这些培养神经元中的苯二氮䓬受体即使不总是,也常常与一种几乎普遍存在的GABA介导的功能,即氯离子电导的激活相偶联。递质信号用于抑制神经元兴奋性,并受到具有临床重要性的苯二氮䓬类药物的促进。在此,我们综述一些关于苯二氮䓬类药物对膜兴奋性药理作用的细节。