Mally J, Connick J H, Stone T W
Department of Pharmacology, University of Glasgow, U.K.
Brain Res. 1990 Oct 22;530(2):353-7. doi: 10.1016/0006-8993(90)91311-4.
The effects of chronic treatment of mice with clonazepam have been examined on the responses of neocortical slices to adenosine, 5-hydroxytryptamine (5-HT) and gamma-aminobutyric acid (GABA). Responses to these agonists were measured as changes in the depolarisation induced by N-methyl-D-aspartate (NMDA). Added to the superfusion medium diazepam blocked responses to adenosine but not 5-HT; this effect was not observed with 2-chloroadenosine or in the presence of 2-hydroxynitrobenzylthioguanosine. GABA was inactive in control slices but chronic treatment with clonazepam induced responses to GABA and enhanced responses to adenosine but not 5-HT. It is suggested that the induction of GABA responses may reflect the up-regulation of GABA receptors, but the increase of adenosine responses by clonazepam implies that there is no simple relationship between adenosine receptor binding and functional responses.
已研究了用氯硝西泮长期治疗小鼠对新皮质切片对腺苷、5-羟色胺（5-HT）和γ-氨基丁酸（GABA）反应的影响。这些激动剂的反应通过N-甲基-D-天冬氨酸（NMDA）诱导的去极化变化来测量。添加到灌流培养基中的地西泮可阻断对腺苷的反应，但不阻断对5-HT的反应；2-氯腺苷或在2-羟基硝基苄基硫代鸟苷存在的情况下未观察到这种效应。GABA在对照切片中无活性，但用氯硝西泮长期治疗可诱导对GABA的反应，并增强对腺苷的反应，但不增强对5-HT的反应。提示GABA反应的诱导可能反映了GABA受体的上调，但氯硝西泮增加腺苷反应意味着腺苷受体结合与功能反应之间不存在简单关系。
