Chronic pain often develops in the orofacial region after inferior alveolar nerve (IAN) injury. In animal models IAN injury often causes severe neuropathic pain-like behavior in the IAN-innervated region as well as the adjacent region that includes the whisker pad skin. However, the basis for the spreading of pain to adjacent facial areas after IAN injury is still unknown. In this study we determined if the transient receptor potential vanilloid 1 (TRPV1) was associated with altered nocifensive behavior evoked by stimulation of the whisker pad skin following IAN transection. Grooming behavior after capsaicin injection into the whisker pad region was significantly increased after IAN transection and the increase in the behavior was reversed by systemic administration of a TRPV1 antagonist. The number of phosphorylated extracellular signal-regulated kinase immunoreactive (IR) neurons in trigeminal spinal subnucleus caudalis and upper cervical spinal cord following capsaicin injection into the whisker pad region was significantly greater in IAN-transected rats than sham-operated rats. The number of TRPV1-IR trigeminal ganglion (TG) neurons innervating the whisker pad skin was also increased significantly after IAN transection. The present findings suggest that an increase in TRPV1 expression in TG neurons innervating the whisker pad skin after IAN transection may underlie the spreading of pain to the adjacent whisker pad skin.
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