Avidor-Reiss T, Zippel R, Levy R, Saya D, Ezra V, Barg J, Matus-Leibovitch N, Vogel Z
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
FEBS Lett. 1995 Mar 13;361(1):70-4. doi: 10.1016/0014-5793(95)00154-2.
The opioid receptors mu, delta and kappa have recently been cloned. Here we show that kappa-agonists inhibit adenylyl cyclase activity in Chinese hamster ovary cells stably transfected with rat kappa-opioid receptor cDNA. Chronic exposure of the cells to kappa-agonists did not lead to significant desensitization of the capacity of the agonists to inhibit adenylyl cyclase. On the other hand, withdrawal of the agonist following the chronic treatment led to the phenomenon of supersensitivity ('overshoot') of adenylyl cyclase activity. Both the inhibition of adenylyl cyclase activity by the acute opioid treatment and the chronic agonist-induced supersensitivity are pertussis toxin sensitive, demonstrating involvement of Gi/Go proteins in both processes.
阿片受体μ、δ和κ最近已被克隆。在此我们表明，κ激动剂可抑制稳定转染大鼠κ阿片受体cDNA的中国仓鼠卵巢细胞中的腺苷酸环化酶活性。细胞长期暴露于κ激动剂不会导致激动剂抑制腺苷酸环化酶的能力出现明显脱敏。另一方面，长期处理后去除激动剂会导致腺苷酸环化酶活性超敏（“过冲”）现象。急性阿片处理对腺苷酸环化酶活性的抑制以及慢性激动剂诱导的超敏反应均对百日咳毒素敏感，表明Gi/Go蛋白参与了这两个过程。
