NDLI: Contribution of GIRK2-mediated postsynaptic signaling to opiate and $α_{2}-adrenergic$ analgesia and analgesic sex differences

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Contribution of GIRK2-mediated postsynaptic signaling to opiate and $α_{2}-adrenergic$ analgesia and analgesic sex differences

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Contribution of GIRK2-mediated postsynaptic signaling to opiate and $α_{2}-adrenergic$ analgesia and analgesic sex differences

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jan, Lily Y. Stoffel, Markus Basbaum, Allan I. Mitrovic, Igor Bader, Semon Margeta-mitrovic, Marta
Description	Author Affiliation: Mitrovic I ( Department of Physiology, University of California, San Francisco, 94143, USA.);
Abstract	The analgesia produced by inhibitory G protein-coupled receptor agonists involves coordinated postsynaptic inhibition via G protein-coupled inwardly rectifying potassium channels (GIRKs) and presynaptic inhibition of neurotransmitter release through regulation of voltage-gated Ca(2+) channels. Here, we used mice lacking the GIRK2 channel subunit to assess the relative contribution of these two effector systems to nociceptive processing in male and female mice. Compared with female WT mice, male WT mice exhibited higher pain thresholds and enhanced opioid (morphine) and alpha(2)-adrenergic (clonidine) receptor-induced antinociception in a spinal reflex test. The GIRK2-null mutation reduced the 'pain' threshold in male but not in female mice, effectively eliminating the sex differences in pain threshold. In addition, deletion of GIRK2 channels in mutant mice largely eliminated clonidine antinociception and significantly decreased morphine antinociception. Furthermore, the more pronounced morphine and clonidine-induced antinociception in male mice disappeared in the GIRK2 mutants. Based on the almost complete loss of clonidine-induced antinociception in the mutant mice, we conclude that it is primarily mediated by postsynaptic alpha(2)-adrenergic receptors. In contrast, the significant residual morphine effect in the mutant mice points to the presynaptic mu opioid receptor as a major contributor to its analgesic action. Finally, our results suggest that the reduced pain responsiveness of male compared with female mice results in part from GIRK2-coupled postsynaptic receptors that are activated by endogenous antinociceptive systems.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	1
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adrenergic Alpha-Agonists Pharmacology Analgesics Clonidine Morphine Pain Physiopathology Potassium Channels, Inwardly Rectifying Potassium Channels Physiology Synapses Analgesia Animals G Protein-Coupled Inwardly-Rectifying Potassium Channels Ganglia, Spinal Mice Mice, Inbred C57BL Mice, Inbred Strains Mice, Knockout Genetics Pain Threshold Deficiency Protein Subunits Sex Characteristics Signal Transduction Spinal Cord Comparative Study Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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