2019 Volume 47 Issue 2 Pages 34-40
Clinically, trigeminal nerve injury sometimes causes persistent orofacial pain. To develop an appropriate treatment for orofacial neuropathic pain, the mechanisms underlying pathological pain need to be elucidated. However, the exact mechanism remains unknown. Here, we examined the involvement of interferon gamma (IFN-γ) signaling in the trigeminal spinal subnucleus caudalis (Vc) in orofacial mechanical hypersensitivity associated with trigeminal nerve injury. Male Sprague Dawley rats (200-250 g) were used in this study. Infraorbital nerve injury (IONI) was established by partial infraorbital nerve ligation under deep anesthesia. The head withdrawal threshold (HWT) in response to mechanical stimulation of the whisker pad skin was measured before and on day 3 after IONI or a sham treatment. The HWTs were also measured on days 1, 2 and 3 following the continuous intra cisterna magna (i.c.m.) administration of IFN-γ (10 μg/3 days) in naive rats. Moreover, the localization of the IFN-γ receptor in the Vc was evaluated on day 3 after IONI or sham treatment. The HWT was decreased on day 3 after IONI. The i.c.m. administration of IFN-γ decreased the HWT in naive rats. In the Vc, the IFN-γ receptor was expressed in Iba-1-labeled cells, and the area occupied by the Iba-1-labeled cells was much larger than that observed in sham rats. The area of Iba1-immunoreactive cells in the superficial laminae of Vc was significantly increased in the IONI model. The present findings suggest that he expression of IFN-γ signals in microglia is a key mechanism underlying orofacial neuropathic pain associated with trigeminal injury.
