Upregulation of Nav1.8 in demyelinated facial nerves might be relevant to the generation of hemifacial spasm.

Abstract

Our previous studies demonstrated that the abnormal muscle response could vanish when the ipsilateral superior cervical ganglion was removed and reappear when norepinephrine was dripped at the neurovascular conflict site. Evidentially, we believed that the mechanism of hemifacial spasm should involve emersion of ectopical action potential in the compressed facial nerve fibers. As the action potential is ignited by ion channel opening, we focused on Nav1.8 that has been found overexpressed in peripheral nerve while damaged. In this study, Moller model was adopted, 20 Sprague-Dawley rats underwent drip of norepinephrine, and the abnormal muscle response wave was monitored in 14 rats. Antibodies against unique epitopes of the α subunit of sodium channel isoforms were used to detect the Nav1.8 neuronal isoforms, and the immunohistochemistry showed strong staining in 13 rats, which were all in the abnormal muscle response positive group (P < 0.05). Accordingly, we concluded that the substance of hemifacial spasm is an ectopic action potential that emerged on the damaged facial nerve, which might be coupled by Nav1.8.