GABA_B受体与腺苷酸环化酶偶联环节的脱敏研究  

STUDIES ON DESENSIZATON OF GABA_B RECEPTOR COUPLED ADENYLATE CYCLASE

作　　者：俞在芳[1] 程冠军[2] 胡本荣[3] 

机构地区：[1]上海医科大学医学神经生物学国家重点实验室,上海200032 [2]中山医科大学肿瘤研究所,广州510089 [3]中山医科大学药理教研室,广州510089

出　　处：《生理学报》1997年第1期25-30,共6页Acta Physiologica Sinica

摘　　要：将突触体膜与佛波酯（PMA），GABAB受体激动剂巴氯芬（Baclofen，BAL）预孵育一定时间后，BAL对腺苷酸环化酶（AC）基础活性及forskolin刺激的AC活性的抑制率显著降低（脱敏）；而forskolin预孵育时，BAL对基础及forskolin刺激的AC活性的抑制率不变，表明GANAB受体与AC偶联环节的脱敏机制涉及蛋白激酶C（PKC）激活，而与蛋白激酶A无关，脱敏时GABAB受体的Kd值增加。本实验提示，可能由于PKC激活导致GABAB受体结构或构象改变，使受体-G蛋白脱偶联而出现脱敏现象。After preincubation of crude synaptic membranes (P2 membranes) with phorber ester (PMA) or GABAB receptor agonist baclofen (BAL), the rate of inhibition of BALon basal adenylate cyclase (AC) activity and forskolin-stimulated AC activity significantly reduced (desensitized). This effect of BAL did not change after preincubationwith forskolin suggesting that the desensitization mechanism of GABAB receptor coupledAC is related with activation of protein kinase C (PKC), but not with protein kinaseA. It was further found that the equilibrium dissociation constant (Kd) of GABAB receptor was increased during desensitization. Our results suggest that PKC activationmay cause some structural or conformational changes of GABAB receptor, resulting inan uncoupling from G protein and desensitization of GABAB receptor-coupled AC.

关 键 词：神经受体 γ氨基丁酸受体 腺苷酸环化酶 脱敏 

分 类 号：R338[医药卫生—人体生理学]