Ueda H, Miyamae T, Fukushima N, Misu Y
Department of Pharmacology, Yokohama City University School of Medicine, Japan.
Neuroreport. 1994 Oct 3;5(15):1985-8. doi: 10.1097/00001756-199410000-00037.
In Xenopus oocytes injected with RNA coding for the delta-opioid receptor a small chloride current was evoked by [D-Ala2,Ser5]leucine-enkephaline-Thr6 (DSLET), a delta 2-opioid agonist. The evoked currents were rapidly reduced upon repeated challenges of DSLET. When Gil alpha RNA was co-injected into the oocyte, the evoked currents were increased 3.8-fold and became constant after at least three repeated challenges. In oocytes injected with RNAs coding for delta-receptor and Gil alpha, pretreatment with K-252a, a potent inhibitor of protein kinases, further potentiated the delta-receptor-mediated current responses, compared with those without the inhibitor. These results suggest that signalling involving the delta-opioid receptor is inactivated through in vivo phosphorylation in the Xenopus oocyte.
在注射了编码δ-阿片受体RNA的非洲爪蟾卵母细胞中,δ2-阿片激动剂[D-丙氨酸2,丝氨酸5]亮氨酸脑啡肽-苏氨酸6(DSLET)可诱发微小的氯离子电流。重复给予DSLET刺激时,诱发电流迅速减小。当将Gαi1 RNA共注射到卵母细胞中时,诱发电流增加了3.8倍,并且在至少三次重复刺激后变得稳定。在注射了编码δ-受体和Gαi1 RNA的卵母细胞中,与未使用抑制剂的情况相比,用蛋白激酶的强效抑制剂K-252a预处理可进一步增强δ-受体介导的电流反应。这些结果表明,在非洲爪蟾卵母细胞中,涉及δ-阿片受体的信号传导通过体内磷酸化而失活。