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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Acute ethanol administration affects memory reactivation: A look at the neuronal density and apoptosis in the rat hippocampus
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Acute ethanol administration affects memory reactivation: A look at the neuronal density and apoptosis in the rat hippocampus

机译：急性乙醇给药影响记忆激活：从大鼠海马神经元密度和细胞凋亡的角度看

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This study is an attempt to examine whether administration of ethanol after memory reactivation will modulate expression of memory in rats or not. We further examined whether this administration alters the number of tunnel positive cells in hippocampus. Adult male Wistar rats were trained in a fear conditioning system using two 1 s , 0.6 mA shock with an interval of 180 s. 24 h later the rats were returned to the chamber for reactivation, and then they were injected with ethanol (0.5, 1, 1.5 mg/kg) or saline, ip. Again, one, seven and fourteen days after reactivation, the rats were returned to the context for 5 min. The freezing time (absence of all movements except respiration) was scored in seconds. In the second experiment, after test 1, the animals were anesthetized and a transcardial perfuse with phosphate buffer and paraformaldehyde 4% was conducted. After post-fixation of brains 5-μm sections were stained with cresyl violet. Finally, paraffin-embedded sections of 10 μm were cut out throughout the tissue and each sample was processed with TUNEL. The number of apoptotic cells in a 130 μm-long segment of the hippocampal CA1 and CA3 fields and dentate gyrus was counted. The data demonstrate that ethanol exposure impairs post retrieval processes. Rats receiving ethanol (1.5 mg/kg) showed lower freezing levels during the first test. Moreover, ethanol decreases the density of CA1, CA3 and DG cells and increases the density of apoptotic cells in all regions of hippocampus. Therefore, ethanol exposure impairs reconsolidation of contextual fear conditioning probably via decreasing the density of CA1, CA3 and DG cells.
机译：这项研究是试图检查记忆重新激活后给予乙醇是否会调节大鼠记忆的表达。我们进一步检查了这种给药方式是否会改变海马中隧道阳性细胞的数量。成年雄性Wistar大鼠在恐惧条件调节系统中接受两次1 s，0.6 mA电击，间隔180 s的训练。 24小时后，将大鼠返回到小室中重新激活，然后向它们注射乙醇（0.5、1、1.5 mg / kg）或生理盐水。再次激活后1、7和14天，将大鼠放回原处5分钟。冻结时间（除了呼吸外，没有其他动作）以秒计。在第二个试验中，在试验1之后，将动物麻醉，并用磷酸盐缓冲液和4％的多聚甲醛进行经心灌注。脑固定后，将5-μm切片用甲苯磺酰紫染色。最后，在整个组织中切出10μm的石蜡包埋切片，并用TUNEL处理每个样品。计数海马CA1和CA3区域和齿状回的130μm长段中的凋亡细胞数。数据表明，乙醇暴露会损害后期检索过程。接受乙醇（1.5 mg / kg）的大鼠在第一次测试中显示出较低的冻结水平。此外，乙醇会降低海马所有区域中CA1，CA3和DG细胞的密度，并增加凋亡细胞的密度。因此，乙醇暴露可能通过降低CA1，CA3和DG细胞的密度来削弱情境恐惧条件的巩固。

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