oxytocin and Nociceptive-Pain

The treatment of chronic pain arising from deep tissues is currently inadequate and there is need for new pharmacological agents to provide analgesia. The endogenous paracrine hormone/neurotransmitter oxytocin is intimately involved in the modulation of multiple physiological and psychological functions. Recent experiments have given clear evidence for a role of oxytocin in the modulation of nociception. The present article reviews the existent human and basic science data related to the direct and indirect effects of oxytocin on pain. Due to its analgesic, anxiolytic, antidepressant and other central nervous system effects, there is strong evidence that oxytocin and other drugs acting through the oxytocin receptor could act as multifunctional analgesics with unique therapeutic value.

Topics: Analgesics; Animals; Chronic Pain; Humans; Nociceptive Pain; Oxytocics; Oxytocin; Pain Management

Topics: Acute Disease; Afferent Pathways; Animals; Arginine Vasopressin; Arthritis; Corticotropin-Releasing Hormone; Hypothalamo-Hypophyseal System; Male; Neurons; Nociceptive Pain; Osteoarthritis, Knee; Oxytocin; Pituitary-Adrenal System; Pro-Opiomelanocortin; Rats; Rats, Wistar

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

Topics: Acetic Acid; Acid Sensing Ion Channel Blockers; Acid Sensing Ion Channels; Action Potentials; Analgesics; Animals; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Ganglia, Spinal; Mice, Inbred C57BL; Mice, Knockout; Nociception; Nociceptive Pain; Oxytocin; Rats, Sprague-Dawley; Receptors, Vasopressin; Sensory Receptor Cells