Extensive neuronal cell death following intracranial transection of the facial nerve in the adult rat.

The aim of the present study is to examine the neuronal degeneration and the glial response following intracranial transection of the facial nerve close to the brainstem and furthermore to compare the results with a distal nerve injury. The facial nerve was cut either intracranially in the posterior cranial fossa or further distally, where it passes the parotid gland, in adult rats. Intracranial axotomy caused a massive loss of neuronal profiles. Only 26.8+/-11.3% of facial motor neuronal profiles were found ipsilateral to the nerve injury when compared to the contralateral side, following intracranial axotomy. This was statistically significant in comparison to the distal injury (72.4+/-9.5%), 4 weeks post-lesion. Reactive microglial cells expressed ED1 immunoreactivity following the intracranial axotomy but not following the distal nerve injury. In conclusion, there was a large discrepancy in neuronal degeneration as well as presence of phagocytic (ED1 positive) microglia between the two lesions. The intracranial lesion model used in the present study generates a massive neuronal cell death and should therefore be a useful tool for studies on proximal cranial nerve injuries and in particular mechanisms causing cell death, which may occur following, for example, head trauma.