Nimodipine-induced improved survival rate of facial motor neurons following intracranial transection of the facial nerve in the adult rat.
OBJECTIVE
Neuronal survival is an important factor in the achievement of functional 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 to L-type voltage-gated calcium channels, has been shown to be neuroprotective in various lesion models of the central and peripheral nervous systems. The aim of the present study was to evaluate the effect of nimodipine on motor neuron survival in the facial motor nucleus following intracranial transection of the adult rat facial nerve.


METHODS
The facial nerve was cut intracranially in the posterior cranial fossa. Nimodipine was administered orally preoperatively for 3 days and postoperatively 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 month postinjury in animals treated with nimodipine (61+/-6.7%) in comparison with untreated animals (26.8+/-11.3%). Immunocytochemical analysis showed an increase in the amount of OX42 (microglia), ED1 (macrophages), and anti-glial fibrillary acidic protein (astrocytes) ipsilateral to the nerve injury; 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, which may be useful as a "cranial nerve protective agent" following insults such as head injury or skull base surgery.
Mattsson
P
P
Department of Clinical Neuroscience, Karolinska Hospital, Stockholm, Sweden. perm@neuro.ks.se
Aldskogius
H
H
Svensson
M
M
D000284:Administration, Oral; D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000473:pathology; D001933:Brain Stem / Q000187:drug effects / Q000601:surgery*; D002121:Calcium Channel Blockers / Q000008:administration & dosage / Q000627:therapeutic use*; D002452:Cell Count; D002470:Cell Survival; D003388:Cranial Fossa, Posterior; D005154:Facial Nerve / Q000187:drug effects* / Q000473:pathology / Q000601:surgery; D005158:Facial Paralysis / Q000517:prevention & control; D005500:Follow-Up Studies; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D007150:Immunohistochemistry; D008264:Macrophages / Q000187:drug effects / Q000473:pathology; D008297:Male; D017628:Microglia / Q000187:drug effects / Q000473:pathology; D009046:Motor Neurons / Q000187:drug effects* / Q000473:pathology; D009434:Neural Pathways / Q000187:drug effects / Q000601:surgery; D009457:Neuroglia / Q000187:drug effects / Q000473:pathology; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D009553:Nimodipine / Q000008:administration & dosage / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley
D002121:Calcium Channel Blockers; D005904:Glial Fibrillary Acidic Protein; D018696:Neuroprotective Agents; D009553:Nimodipine