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Korean J Physiol Pharmacol. 2018 Mar;22(2):173-182. doi: 10.4196/kjpp.2018.22.2.173. Epub 2018 Feb 23.

Oxytocin produces thermal analgesia via vasopressin-1a receptor by modulating TRPV1 and potassium conductance in the dorsal root ganglion neurons.

Author information

1
Neuroscience Research Institute and Department of Physiology, Korea University College of Medicine, Seoul 02841, Korea.
2
Department of Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Seoul 03080, Korea.
3
Dental Research Institute and Department of Neurobiology & Physiology, School of Dentistry, Seoul National University, Seoul 08826, Korea.
4
Department of Physiology, College of Medicine, Gachon University, Incheon 21936, Korea.
5
Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, Osaka 565-0871, Japan.

Abstract

Recent studies have provided several lines of evidence that peripheral administration of oxytocin induces analgesia in human and rodents. However, the exact underlying mechanism of analgesia still remains elusive. In the present study, we aimed to identify which receptor could mediate the analgesic effect of intraperitoneal injection of oxytocin and its cellular mechanisms in thermal pain behavior. We found that oxytocin-induced analgesia could be reversed by d(CH2)5[Tyr(Me)2,Dab5] AVP, a vasopressin-1a (V1a) receptor antagonist, but not by desGly-NH2-d(CH2)5[DTyr2, Thr4]OVT, an oxytocin receptor antagonist. Single cell RT-PCR analysis revealed that V1a receptor, compared to oxytocin, vasopressin-1b and vasopressin-2 receptors, was more profoundly expressed in dorsal root ganglion (DRG) neurons and the expression of V1a receptor was predominant in transient receptor potential vanilloid 1 (TRPV1)-expressing DRG neurons. Fura-2 based calcium imaging experiments showed that capsaicin-induced calcium transient was significantly inhibited by oxytocin and that such inhibition was reversed by V1a receptor antagonist. Additionally, whole cell patch clamp recording demonstrated that oxytocin significantly increased potassium conductance via V1a receptor in DRG neurons. Taken together, our findings suggest that analgesic effects produced by peripheral administration of oxytocin were attributable to the activation of V1a receptor, resulting in reduction of TRPV1 activity and enhancement of potassium conductance in DRG neurons.

KEYWORDS:

Dorsal root ganglion; Electrophysiology; Oxytocin; Pain; Vasopressin receptor

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