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

周围神经损伤后，大鼠面神经核团内降钙素基因相关肽（calcitonin gene-related peptide，CGRP）、即刻早期基因（immediate early gene，c-jun）和生长相关蛋白（growth associated protein，B-50）mRNA表达增加。对神经的直接损伤被认为诱导这些神经活性物质的基因表达的变化，其可能在对损伤的适应性反应、神经元存活、生长和再生中起作用。本研究采用选择性栓塞技术建立周围性面神经麻痹的缺血性动物模型。在该模型中，面瘫持续约3天，并恢复无任何神经元缺损。应用原位杂交技术观察面神经核团CGRP、c-jun和GAP-43 mRNA的表达。这些mRNA在栓塞后第1天开始升高，持续1周后逐渐下降。结果提示，缺血性面神经麻痹可诱导CGRP、c-jun和GAP-43在胞体中表达，其表达水平和持续时间与直接神经损伤模型不同。

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.