Psychiatry & Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Rd., Stanford, CA 94305, USA.
Pharmacol Biochem Behav. 2011 Sep;99(3):428-36. doi: 10.1016/j.pbb.2011.03.002. Epub 2011 Mar 23.
Despite extensive description of the damaging effects of chronic alcohol exposure on brain structure, mechanistic explanations for the observed changes are just emerging. To investigate regional brain changes in protein expression levels following chronic ethanol treatment, one rat per sibling pair of male Wistar rats was exposed to intermittent (14 h/day) vaporized ethanol, the other to air for 26 weeks. At the end of 24 weeks of vapor exposure, the ethanol group had blood ethanol levels averaging 450 mg%, had not experienced a protracted (> 16 h) withdrawal from ethanol, and revealed only mild evidence of hepatic steatosis. Extracted brains were micro-dissected to isolate the prefrontal cortex (PFC), dorsal striatum (STR), corpus callosum genu (CCg), CC body (CCb), anterior vermis (AV), and anterior dorsal lateral cerebellum (ADLC) for protein analysis with two-dimensional gel electrophoresis. Expression levels for 54 protein spots were significantly different between the ethanol- and air-treated groups. Of these 54 proteins, tandem mass spectroscopy successfully identified 39 unique proteins, the levels of which were modified by ethanol treatment: 13 in the PFC, 7 in the STR, 2 in the CCg, 7 in the CCb, 7 in the AV, and 5 in the ADLC. The functions of the proteins altered by chronic ethanol exposure were predominantly associated with neurotransmitter systems in the PFC and cell metabolism in the STR. Stress response proteins were elevated only in the PFC, AV, and ADLC perhaps supporting a role for frontocerebellar circuitry disruption in alcoholism. Of the remaining proteins, some had functions associated with cytoskeletal physiology (e.g., in the CCb) and others with transcription/translation (e.g., in the ADLC). Considered collectively, all but 4 of the 39 proteins identified in the present study have been previously identified in ethanol gene- and/or protein-expression studies lending support for their role in ethanol-related brain alterations.
尽管慢性酒精暴露对大脑结构的破坏性影响已有广泛描述,但观察到的变化的机制解释才刚刚出现。为了研究慢性乙醇处理后蛋白质表达水平的区域性大脑变化,每对雄性 Wistar 大鼠的一个同胞兄弟被暴露于间歇性(每天 14 小时)蒸发的乙醇中,另一个暴露于空气中 26 周。在暴露于蒸气 24 周结束时,乙醇组的血液乙醇水平平均为 450mg%,没有经历过长时间(> 16 小时)的乙醇戒断,并且仅显示出轻微的肝脂肪变性的证据。提取的大脑被微解剖以分离前额叶皮层(PFC)、背侧纹状体(STR)、胼胝体膝部(CCg)、胼胝体体部(CCb)、前蚓部(AV)和前背外侧小脑(ADLC),用于二维凝胶电泳的蛋白质分析。与空气处理组相比,54 个蛋白质斑点的表达水平有显著差异。在这 54 种蛋白质中,串联质谱成功鉴定了 39 种独特的蛋白质,其水平被乙醇处理改变:13 种在 PFC 中,7 种在 STR 中,2 种在 CCg 中,7 种在 CCb 中,7 种在 AV 中,5 种在 ADLC 中。慢性乙醇暴露改变的蛋白质的功能主要与 PFC 中的神经递质系统和 STR 中的细胞代谢有关。应激反应蛋白仅在 PFC、AV 和 ADLC 中升高,这可能支持额-小脑电路中断在酒精中毒中的作用。在其余的蛋白质中,一些具有与细胞骨架生理学相关的功能(例如在 CCb 中),而另一些具有转录/翻译功能(例如在 ADLC 中)。总体而言,本研究中鉴定的 39 种蛋白质中,除 4 种外,其余均已在乙醇基因和/或蛋白质表达研究中被鉴定,支持它们在与乙醇相关的大脑改变中的作用。