Proteomic analysis in the rat cerebellar flocculus during vestibular compensation

采用大鼠单侧前庭大肌切除术（UL）作为人类眩晕模型。在该模型中，自发性眼球震颤和由UL引起的平衡失调在48-72小时内得到改善。这种改善，称为前庭补偿（VC），是持久的。虽然小脑绒球已被报道参与VC，VC背后的分子机制仍然是未知的。在这里，我们使用2D-DIGE来描述导致VC急性（48小时）和慢性（1周）阶段的絮状物中的蛋白质变化。结果，我们发现967个蛋白质斑点中有99个在其强度上显示出显著变化。利用MALDI-TOF MS，我们成功地鉴定了10个蛋白质，如N-乙基马来酰亚胺敏感融合蛋白（Nsf）。其中，翻译后修饰参与VC急性期的可能性被提出，NSF能够认为进行了翻译后修饰的磷酸化。

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.