Proteomic analysis in the rat cerebellar flocculus during vestibular compensation

采用大鼠单侧迷路切除术(UL)建立人类眩晕模型。在该模型中，UL引起的自发性眼球震颤和平衡失调在48-72小时内得到改善。这种改善被称为前庭补偿(VC)，是长期存在的。虽然已有报道称小脑小叶参与了VC的发病，但VC背后的分子机制仍不清楚。在这里，我们使用2D-DGE来描述导致VC急性期(48小时)和慢性期(1周)的小叶蛋白变化。结果，我们发现967个蛋白点中有99个的强度发生了显著变化。利用MALDI-TOF MS，我们成功鉴定了N-乙基马来酰亚胺敏感融合蛋白(NSF)等10种蛋白质。其中，翻译后修饰参与了VC急性期的可能性，NSF能够认为翻译后修饰进行了磷酸化。

Unilateral labyrinthectomy (UL) in rats is used as a human vertigo model. In this model, spontaneous nystagmus and dysequilibrium caused by UL are ameliorated within 48-72 hours. This amelioration, named vestibular compensation (VC), is long lasting. Although cerebellar flocculi have been reported to be involved in VC, the molecular mechanism behind VC is still unknown. Here, we used 2D-DIGE to depict protein changes in flocculi that contribute to acute (48 hours) and chronic (1 week) stages of VC. As a result, we found that 99 out of 967 protein spots showed significant changes in their intensities. Using MALDI-TOF MS, we successfully identified 10 proteins, such as N-ethylmaleimide-sensitive fusion protein (Nsf). Among these, a possibility that posttranslational modification was participating in the acute stage of VC was suggested, and NSF was able to consider that phosphorylation of the posttranslational modification was carried out.