Franke H, Kittner H, Berger P, Wirkner K, Schramek J
Institute of Pharmacology and Toxicology, University of Leipzig, Germany.
Alcohol. 1997 Sep-Oct;14(5):445-54. doi: 10.1016/s0741-8329(96)00209-1.
Chronic ethanol treatment of Wistar rats to 10% (v/v) ethanol over a period of 4, 12, and 36 weeks produced distinct alterations of the glial fibrillary acidic protein immunoreactivity (GFAP-IR) of dorsal hippocampal astrocytes. Ethanol consumption over a period of 4 weeks caused an increase in the total GFAP-IR of the astrocytes. Down-regulation of the total GFAP-IR was measured in all examined brain regions after 36 weeks of ethanol treatment. Prolonged ethanol treatment induced a significant loss of the total number of hippocampal pyramidal and dentate gyrus granule cells. Regional differences in the vulnerability to the neurotoxic effects of chronic ethanol intake over 36 weeks were found: CA3 > CA1 + CA2 > > CA4 > GD. In agreement with the degree of neuronal cell loss, ethanol-induced behavioral impairments were found. The acquisition of maze performance using a complex elevated labyrinth was deteriorated after 36 weeks of ethanol treatment, suggesting a deficit in learning and memory. These findings illustrate the importance of time-response analysis when determining the structural and functional changes produced by chronic ethanol treatment.
将Wistar大鼠在4周、12周和36周的时间内用10%（体积/体积）乙醇进行慢性乙醇处理，会使背侧海马星形胶质细胞的胶质纤维酸性蛋白免疫反应性（GFAP-IR）产生明显改变。4周的乙醇摄入导致星形胶质细胞的总GFAP-IR增加。乙醇处理36周后，在所有检测的脑区均检测到总GFAP-IR下调。长期乙醇处理导致海马锥体细胞和齿状回颗粒细胞总数显著减少。发现了在36周慢性乙醇摄入的神经毒性作用下不同脑区的易损性差异：CA3 > CA1 + CA2 > > CA4 > 齿状回。与神经元细胞丢失程度一致，发现了乙醇诱导的行为障碍。使用复杂高架迷宫进行迷宫行为表现的获取在乙醇处理36周后变差，表明学习和记忆存在缺陷。这些发现说明了在确定慢性乙醇处理产生的结构和功能变化时进行时间反应分析的重要性。
