[Mutual interaction of vestibular afferent nervous system and vestibular efferent nervous system in vestibular compensation].

OBJECTIVE: To study the mutual interaction of vestibular afferent nervous system and vestibular efferent nervous system in vestibular compensation. METHODS: Build up animal model of vestibular compensation by destroying single side vestibule of wistar rat. In the study the rats were divided into 3 groups: Group A 16 normal rats; Group B 15 rats, after 7 days of left vestibular damage; Group C 7 rats 3 months after left vestibular damage; and Group D 7 rats, after vestibular compensation. Electromyography of the rats was recorded and the expression of calcitonin gene relative peptide (CGRP), choline acetyltransferase (AChT) and Na-K-ATPase were investigated in efferent vestibular nervous system. RESULTS: Electric potential activity of muscles of injury side decreased while that of the opposite side increased. In animals of vestibular compensation electric potential of bilateral musculus longus capitis at quiescent stage recovered symmetrically. CGRP positive cells of efferent vestibular nervous system increased bilaterally, and their activity enhanced, especially obvious at the acute stage. AChT positive cells of injury side of efferent vestibular nervous system decreased, but reaction degree of two sides enhanced. Reaction degree of the opposite side enhanced obviously at the stage of vestibular compensation. Expression of Na-K-ATPase mRNA of the same side was lower, but vestibular signal of the opposite side enhanced, clinically head and neck inclined obliquely by means of medial fasciculus of tractus vestibulospinalis. Months later, vestibular signal of the same side enhanced, and that of the opposite side enhanced also, clinical symptoms improved slightly. At the vestibular compensation stage, expression of Na-K-ATPase mRNA of the same side enhanced, and it was same as that of the opposite side or much higher, clinically it reached vestibular compensation. CONCLUSION: Comprehensive effect of the above results maybe as follows: Efferent vestibular nervous system inhibited afferent signal of the opposite vestibule, and it modulated excitement of vestibular center of the same side, and it worked in the complicated mechanisms of vestibular compensation. CGRP may have facilitation function to the vestibular afferent signal of injury side. While Ach improved vestibule compensation by means of inhibition of vestibule excitement of the healthy side.

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

BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.