Nimodipine-induced improved survival rate of facial motor neurons following intracranial transection of the facial nerve in the adult rat

Object. Neuronal survival is an important factor in the achievement of func tional restitution after peripheral nerve injuries. Intracranial tumors or trauma may cause patients to exhibit a temporary or permanent facial nerve palsy. Nimodipine, which acts as an antagonist Co L-type voltage gated calc ium channels, has been shown to be neuroprotective in various lesion models of the central and peripheral nervous systems. The aim of the present stud y was to evaluate the effect of nimodipine on motor neuron survival in the facial motor nucleus following intracranial transection of the adult rat fa cial nerve. Methods. The facial nerve was cut intracranially in the posterior cranial f ossa. Nimodipine was administered orally preoperatively for 3 days and post operatively for up to 1 month, after which the number of neuronal profiles was quantified. The glial reaction was studied in the facial nucleus for up to 1 month by using immunocytochemical analysis. There was a significantly larger proportion of surviving motor neurons 1 mo nth postinjury in animals treated with nimodipine (61 +/- 6.7%) in comparis on with untreated animals (26.8 +/- 11.3%). Immunocytochemical analysis sho wed an increase in the amount of OX42 (microglia), EDI (macrophages), and a nti-glial fibrillary acidic protein (astrocytes) ipsilateral to the nerve i njury; however, there was no difference between the two experimental groups of animals 2 to 28 days after surgery. Conclusions. The authors propose a neuroprotective role for nimodipine, whi ch may be useful as a "cranial nerve protective agent" following insults su ch as head injury or skull base surgery.