Apoptosis and expression of BCL-2 in facial motoneurons after facial nerve injury.

Abstract

Apoptosis has been implicated in neuronal degeneration after optic and sciatic nerve injury. The mechanisms contributing to facial motoneuron death are poorly understood. This study investigated the mechanisms underlying facial motoneuronal death and the expression of BCL-2 in facial motoneurons after facial nerve injury. Morphologic changes in the facial motoneurons were examined by light and transmission electron microscopy, and TdT-mediated dUTP-biotin nick end labeling (TUNEL) methods was used. Expression of BCL-2 was studied by immunohistochemistry and in situ hybridization after facial nerve injury. Cell shrinkage, condensed cytoplasm, and apoptotic bodies were demonstrated in numerous cells under light microscopy. The chromatin was condensed and localized to the nuclear envelope, forming a crescent or cap, and the endoplasmic reticulum was still visible but appeared swollen under electron microscopy. In vivo TUNEL staining displayed positive facial motoneurons 7 days after facial nerve transsection. The BCL-2 expression in facial motoneurons declined and reached its lowest level on the fifteenth day (p < 0.05). The reduction in BCL-2 expression after facial nerve transsection close to the facial motoneuron nucleus was greater than that of facial nerve transsection far away from the facial motoneuron nucleus (p < 0.05). BCL-2 expression after crushing of the facial nerve was found to be more intense in comparison with that after nerve transsection at the stylomastoid foramen (p < 0.05). These findings indicated that motoneuron death induced by facial nerve transsection was consistent with the process of apoptosis. The endogenous BCL-2 in these motoneurons may protect facial motoneurons from axotomy-induced cell death.