Oxytocin inhibits the activity of acid-sensing ion channels through the vasopressin, V1A receptor in primary sensory neurons

摘要: Background and Purpose A growing number of studies have demonstrated that oxytocin (OT) plays an analgesic role in modulation nociception pain. Most work to date has focused on the central mechanisms OT analgesia, but little is known about whether peripheral are also involved. Acid-sensing ion channels (ASICs) distributed sensory neurons participate nociception. Here, we investigated effects activity ASICs dorsal root ganglion (DRG) neurons. Experimental Approach Electrophysiological experiments were performed from rat DRG. Nociceptive behaviour was induced by acetic acid rats mice lacking vasopressin, V1A receptors. Key Results OT inhibited functional native ASICs. Firstly, dose-dependently decreased amplitude ASIC currents DRG neurons. Secondly, inhibition mimicked arginine vasopressin (AVP) completely blocked receptor antagonist SR49059, not L-368899. Thirdly, altered acidosis-evoked membrane excitability significantly depolarization action potentials stimuli. Finally, peripherally administered or AVP nociceptive responses intraplantar injection rats. Both effect pain wild-type mice, knockout mice. Conclusions Implications These results reveal a novel mechanism for involving primary mediated receptors.