Oxytocin: pain relief in skin
PAIN, Commentary
Valery Grinevich, Alexandre Charlet

... In this issue of PAIN, González-Hernández et al.1 propose a new site for physiologically relevant oxytocin modulation of nociception: the peripheral nociceptive terminal axons in skin. Asingle subcutaneous administration of oxytocin per se induced a long-lasting (up to 100 minutes) inhibition of nociceptive integration in the spinal cord, as shown through wide-dynamicrange neuron recordings. In a formalin pain model, oxytocin inhibits flinching behavior through peripheral oxytocin receptor activation. Finally, an immunosignal for oxytocin receptor was detected in the nociceptive-specific terminals of the superficial skin layers. Altogether, this combination of approaches and findings indicates that activation of skin-located oxytocin receptor contributes to oxytocin-mediated analgesia.... Click here for more information. 

1 Peripheral oxytocin receptors inhibit the nociceptive input signal to spinal dorsal horn wide-dynamic-range neurons.


Abstract

Oxytocin (OT) has emerged as a mediator of endogenous analgesia in behavioral and electrophysiological experiments. In fact, OT receptors (OTRs) in the spinal dorsal horn participate in a selective inhibition of the neuronal activity mediated by Aδ and C fibers but not Aβ fibers. This study shows that OTRs are expressed in the terminal nerve endings and are able to inhibit nociceptive neuronal firing. Indeed, local peripheral OT blocked the first sensorial activity of Aδ and C fibers recorded in the spinal cord neurons. Furthermore, using the formalin behavioral nociceptive test, we demonstrated that only ipsilateral OTR activation inhibits pain behavior. Our data are reinforced by the fact that the OTR protein is expressed in the sciatic nerve. Consistent with this, immunofluorescence of primary afferent fibers suggest that OTRs could be located in nociceptive-specific terminals of the skin. Taken together, our results suggest that OTRs could be found in nociceptive terminals and that on activation they are able to inhibit nociceptive input.