Expression of sodium channel SNS/PN3 and ankyrin(G) mRNAs in the trigeminal ganglion after inferior alveolar nerve injury in the rat

The inferior alveolar nerve is a sensory branch of the trigeminal nerve tha t is frequently damaged, and such nerve injuries can give rise to persisten t paraesthesia and dysaesthesia. The mechanisms behind neuropathic pain fol lowing nerve injury is poorly understood. However, remodeling of voltage-ga ted sodium channels in the neuronal membrane has been proposed as one possi ble mechanism behind injury-induced ectopic hyperexcitability. The TTX-resi stant sodium channel SNS/PN3 has been implicated in the development of neur opathic pain after spinal nerve injury. We here study the effect of chronic axotomy of the inferior alveolar nerve on the expression of SNS/PN3 mRNA i n trigeminal sensory neurons. The organization of sodium channels in the ne uronal membrane is maintained by binding to ankyrin, which help Link the so dium channel to the membrane skeleton. Ankyrin(G), which colocalizes with s odium channels in the initial segments and nodes of Ranvier, and is necessa ry for normal neuronal sodium channel function, could be essential in the r eorganization of the axonal membrane after nerve injury. For this reason, w e here study the expression of ankyrin(G) in the trigeminal ganglion and th e localization of ankyrin(G) protein in the inferior alveolar nerve after i njury. We show that SNS/PN3 mRNA is down-regulated in small-sized trigemina l ganglion neurons following inferior alveolar nerve injury but that, in co ntrast to the persistent loss of SNS/PN3 mRNA seen in dorsal root ganglion neurons following sciatic nerve injury, the levels of SNS/PN3 mRNA appear t o normalize within a few weeks. We further show that the expression of anky rin(G) mRNA also is downregulated after nerve lesion and that these changes persist for at least 13 weeks. This decrease in the ankyrin(G) mRNA expres sion could play a role in the reorganization of sodium channels within the damaged nerve. The changes in the levels of SNS/PN3 mRNA in the trigeminal ganglion, which follow the time course for hyperexcitability of trigeminal ganglion neurons after inferior alveolar nerve injury, may contribute to th e inappropriate firing associated with sensory dysfunction in the orofacial region. (C) 2000 Academic Press.