Ikeda K, Kobayashi T, Kumanishi T, Niki H, Yano R
Laboratory for Neurobiology of Emotion, RIKEN, Brain Science Institute, Wako, Saitama, Japan.
Neurosci Res. 2000 Sep;38(1):113-6. doi: 10.1016/s0168-0102(00)00144-9.
To investigate the role of G-protein-activated inwardly rectifying K+ (GIRK) channels in opioid-induced analgesia, we compared the effects of opioids in wild-type and weaver mutant mice having mutant GIRK channels. In the tail-flick and hot-plate tests, weaver mutant mice displayed significantly lower analgesia after either morphine or (-)-U-50488 administration. These findings suggest that GIRK channel activation is important in the induction of analgesia by opioids.
为了研究G蛋白激活的内向整流钾离子（GIRK）通道在阿片类药物诱导的镇痛中的作用，我们比较了阿片类药物对野生型小鼠和具有突变GIRK通道的weaver突变小鼠的影响。在甩尾试验和热板试验中，给予吗啡或（-）-U-50488后，weaver突变小鼠的镇痛作用明显较低。这些发现表明，GIRK通道激活在阿片类药物诱导的镇痛中起重要作用。
