Changes in gene expression in facial nerve nuclei in the rat model of ischemic Bell's palsy

众所周知，大鼠周围神经损伤后面神经核中CGRP（降钙素基因相关肽）、c-jun（即早基因）和GAP-43（生长相关蛋白，B-50） mrna的表达增加。神经的直接损伤可引起这些神经活性物质基因表达的变化，这些基因表达的变化可能与神经损伤的适应性反应、神经元的存活、生长和再生有关。本研究采用选择性栓塞技术建立面神经末梢麻痹缺血性动物模型。在该模型中，面部麻痹持续约3天，恢复后无神经元缺损。采用原位杂交技术观察面神经细胞核中CGRP、c-jun和GAP-43 mrna的表达水平。这些mRNA在栓塞后第1天出现升高，持续1周后逐渐降低。结果提示，缺血性面神经麻痹可诱导细胞体细胞中CGRP、c-jun和GAP-43的表达，且这些mrna的表达水平和持续时间不同于直接神经损伤模型。

It is well known that expression of CGRP (calcitonin gene-related peptide) , c-jun (immediate early gene) and GAP-43 (growth-associated protein, B-50) mRNAs increase in the rat facial nerve nuclei after peripheral nerve injury. Direct damage to the nerve is supposed to induce changes in gene expression of these neuroactive substances, which may have roles in adaptive response to the injury, neuronal survival, growth and regeneration. This study was designed to establish ischemic animal model of peripheral facial nerve paralysis with a selective embolization technique. In this model, the paralysis of facial continued for about 3 days and recovered without any neuronal deficit. We observed the levels in CGRP,c-jun and GAP-43 mRNAs in facial nerve nuclei using in situ hybridization. The increase of these mRNA appeared one day after embolization, lasted for 1 week and gradually decreased. The results suggest that the expression of CGRP,c-jun and GAP-43 in cell somata is induced by ischemic facial nerve paralysis, and the level and duration of increase in these mRNAs are different from those in direct nerve injury model.