The K(+) channel GIRK2 is both necessary and sufficient for peripheral opioid-mediated analgesia.

ABSTRACT: The use of opioid agonists acting outside the central nervous system (CNS) is a promising therapeutic strategy for pain control that avoids deleterious central side effects such as apnea and addiction. In human clinical trials and rat models of inflammatory pain, peripherally restricted opioids have repeatedly shown powerful analgesic effects; in some mouse models however, their actions remain unclear. Here, we investigated opioid receptor coupling to K(+) channels as a mechanism to explain such discrepancies. We found that GIRK channels, major effectors for opioid signalling in the CNS, are absent from mouse peripheral sensory neurons but present in human and rat. In vivo transgenic expression of GIRK channels in mouse nociceptors established peripheral opioid signalling and local analges

SUBMITTER: Nockemann D 

PROVIDER: S-EPMC3944465 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature