Department of Pharmacology, Faculty of Science, Prince of Songkla University, Hat-Yai, Thailand.
Acta Histochem. 2011 May;113(3):283-9. doi: 10.1016/j.acthis.2009.11.001. Epub 2010 Jan 6.
The pathology of brain atrophy mediated by alcohol was investigated in all parts of the cerebral cortex (the frontal, parietal, temporal lobes and occipital cortex) by using two markers: parvalbumin (PV) and glial fibrillary acidic protein (GFAP). Three-month old male Wistar rats were divided into control (C) and alcohol-exposed groups. The control group received distilled water, whereas the alcohol-exposed groups received either a low dose (2g/kg body wt) or a high dose (5g/kg) of ethanol for periods of 21 days, 3 or 6 months. The brains of the animals were processed for immunohistochemistry using anti-parvalbumin and anti-GFAP antibodies and the number of PV immunoreactive (PV-ir) neurons and GFAP immunoreactive (GFAP-ir) astrocytes were counted per unit area. Results showed that all groups exposed to ethanol had significantly reduced numbers of PV-ir neurons in all parts of the cerebral cortex compared to those of the control group (p<0.05). In contrast, the numbers of GFAP-ir astrocytes were increased in all parts of the cerebral cortex following the exposure to a high dose of ethanol after 21-days (but not a low dose) and both high and low doses of ethanol after 3-months or 6-months treatment compared to those of age-matched control groups (p<0.05). This indicated that in young rats (21-days), PV-ir neurons in all cerebral cortex areas seemed to be more sensitive to alcohol than GFAP-ir astrocytes. Moreover, the change in densities of both PV-ir neurons and GFAP-ir astrocytes became more apparent after exposure to prolonged and high doses of ethanol. The decrease of PV-ir neurons and the increase of GFAP-ir astrocytes indicated that alcohol may induce pathology in broad areas of the cerebral cortex. This may explain the underlying mechanism of brain atrophy and other impairments found in alcoholics. For investigations of the effects of alcohol on mediating brain pathology, we recommend the use of the two markers (PV and GFAP).
钙结合蛋白（PV）和神经胶质纤维酸性蛋白（GFAP），研究了酒精介导的脑萎缩的病理学。将三个月大的雄性 Wistar 大鼠分为对照组（C）和酒精暴露组。对照组给予蒸馏水，而酒精暴露组给予低剂量（2g/kg 体重）或高剂量（5g/kg）乙醇，持续 21 天、3 个月或 6 个月。对动物的大脑进行免疫组织化学处理，使用抗 PV 和抗 GFAP 抗体，并对每个单位面积的 PV 免疫反应性（PV-ir）神经元和 GFAP 免疫反应性（GFAP-ir）星形胶质细胞的数量进行计数。结果表明，与对照组相比，所有接受乙醇暴露的组在大脑皮层的所有区域中 PV-ir 神经元的数量均显著减少（p<0.05）。相反，在 21 天后暴露于高剂量乙醇后（但低剂量则没有），以及在 3 个月或 6 个月治疗后，高剂量和低剂量乙醇均可使大脑皮层所有区域的 GFAP-ir 星形胶质细胞数量增加，与年龄匹配的对照组相比（p<0.05）。这表明，在幼鼠（21 天）中，所有大脑皮层区域的 PV-ir 神经元似乎比 GFAP-ir 星形胶质细胞对酒精更敏感。此外，在暴露于长时间和高剂量的乙醇后，PV-ir 神经元和 GFAP-ir 星形胶质细胞密度的变化变得更加明显。PV-ir 神经元的减少和 GFAP-ir 星形胶质细胞的增加表明，酒精可能会引起大脑皮层广泛区域的病理学改变。这可以解释酒精中毒患者大脑萎缩和其他损伤的潜在机制。为了研究酒精对介导脑病理学的影响，我们建议使用这两种标志物（PV 和 GFAP）。
