Oxytocin in the paraventricular nucleus attenuates Incision-Induced mechanical allodynia

Abstract

Oxytocin (OT) neurons localized in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) send fibers to the brain and spinal cord. While most previous studies have looked at the role of OT in chronic pain, few have investigated the role of OT in acute pain, particularly postoperative pain. In the present study, the role of OT in incision-induced allodynia was explored for the first time, using a rat incisional pain model. Immunohistochemical staining showed that, compared with the baseline (prior to incision) measurements, the OT content in the PVN was significantly decreased at 0.5, 1.0 and 3.0 h post-incision and returned to the baseline level at 6.0 h post-incision. By contrast, there was no significant difference in the OT content in the SON prior to and subsequent to incision. A dose-dependent inhibition of mechanical hypersensitivity was detected 30 min after intracerebroventricular injection of OT (100, 400 or 600 ng) and lasted for 3.0 h. No significant difference was noted, however, between the intrathecal OT injection group (600 ng) and the control group. In conclusion, the present study provides the first in vivo evidence that OT in the PVN predominantly attenuates incision-induced mechanical allodynia at the supraspinal, rather than the spinal, level. This suggests that OT is involved in supraspinal analgesia for postoperative pain.