Change in gene expression in facial nerve nuclei and the effect of superoxide dismutase in a rat model of ischemic facial paralysis.

Peripheral nerve injury induces changes in gene expressions of a variety of neuroactive substances in cell somata, which may have roles in the adaptive response to the injury, neuronal survival, growth and regeneration. In this study, we designed a rat model of ischemic peripheral facial paralysis with a selective embolization technique, and observed mRNA expression of calcitonin gene-related peptide (CGRP), c-jun, and growth associated protein (GAP)-43 in facial nerve nuclei using in situ hybridization histochemistry. The rats were demonstrated to have a transient facial paralysis consistently, and thus this method was regarded as a model of minor peripheral nerve injury. The mRNA of CGRP, c-jun and GAP-43 showed a distinct pattern of induction and time course of increase after the ischemic nerve injury. The results suggest that the small injury to the peripheral nerve was able to induce changes in mRNA expression in the cell body of motoneurons. We also investigated the protective effect of superoxide dismutase (SOD), which is a free radical-scavenging enzyme involved in cellular antioxidant defenses. The SOD treatment clearly alleviated the behavioral impairment and decreased the CGRP mRNA expression at 3rd day after injury. These data suggest that a free radical generated by the ischemia may be partially responsible for ischemic nerve damage and the change in gene expression in motoneurons.