R082: Intracochlear Trauma Study of In Vitro Implanted Cochlea

Abstract

cascade of secondary processes of delayed and amplified injury to the FMN. Release of fatty acids, in particular arachidonic acid, from cell membranes is believed to be one of the most important mechanisms of neuronal cell death following nerve injury. Mechanisms of neuronal injury induced by fatty acid may include reaction of lipid peroxidation. One of the major biologically active products of arachidonic acid peroxidation is 4-hydroxynonenal (HNE). Inhibition of the lipid peroxidation may protect neuronal cell death produced by retrograde degeneration. METHODS: In 40 adult rats, the right facial nerve was avulsed from stylomastoid foramen. Following nerve avulsion, the effects of a regular dose of vitamin E (20g/mL), and high dose of vitamin E (200g/mL) on HNE activity were investigated using immune-histochemistry. FMN motoneurons and glial cells were counted bilaterally in sections stained with cresyl violet. RESULTS: The number of surviving motoneurons in the ipsilateral FMN was significantly greater among regular dose vitamin E-treated rats than nontreated controls or high dose vitamin Etreated rats following nerve avulsion. The peak of gliosis in cases with regular dose-vitamin E treatment was in the first week, and then it was strongly suppressed after 2nd week. Whereas in high dose-vitamin E treated group, the gliosis was suppressed in 1st week but increased progressively after that. CONCLUSION: The present study demonstrates the neuroprotective effect of vitamin E after peripheral facial nerve avulsion. Antioxidants may have therapeutic potential in traumatic facial nerve dysfunction resulting from head injury, ear surgery and parotid gland surgery. SIGNIFICANCE: Antioxidants may have therapeutic potential in traumatic facial nerve dysfunction resulting from head injury, ear surgery and parotid gland surgery.