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首页> 外文期刊>Alcohol >The role of cortisol in chronic binge alcohol-induced cerebellar injury: Ovine model
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The role of cortisol in chronic binge alcohol-induced cerebellar injury: Ovine model

机译：皮质醇在慢性泪液诱导的小脑损伤中的作用：绵延模型

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摘要

Women who drink alcohol during pregnancy are at high risk of giving birth to children with neurodevelopmental disorders. Previous reports from our laboratory have shown that third trimester equivalent binge alcohol exposure at a dose of 1.75 g/kg/day results in significant fetal cerebellar Purkinje cell loss in fetal sheep and that both maternal and fetal adrenocorticotropin (ACTH) and cortisol levels are elevated in response to alcohol treatment. In this study, we hypothesized that repeated elevations in cortisol from chronic binge alcohol are responsible at least in part for fetal neuronal deficits. Animals were divided into four treatment groups: normal control, pair-fed saline control, alcohol and cortisol. The magnitude of elevation in cortisol in response to alcohol was mimicked in the cortisol group by infusing pregnant ewes with hydrocortisone for 6 h on each day of the experiment, and administering saline during the first hour in lieu of alcohol. The experiment was conducted on three consecutive days followed by four days without treatment beginning on gestational day (GD) 109 until GD 132. Peak maternal blood alcohol concentration in the alcohol group was 239 ± 7 mg/dl. The fetal brains were collected and processed for stereological cell counting on GD 133. The estimated total number of fetal cerebellar Purkinje cells, the reference volume and the Purkinje cell density were not altered in response to glucocorticoid infusion in the absence of alcohol. These results suggest that glucocorticoids independently during the third trimester equivalent may not produce fetal cerebellar Purkinje cell loss. However, the elevations in cortisol along with other changes induced by alcohol could together lead to brain injury seen in the fetal alcohol spectrum disorders.
机译：饮酒在怀孕期间饮酒的妇女患有神经发育障碍儿童的高风险。我们实验室的上一份报告表明，胎儿绵羊中的胎儿胎儿幼儿细胞损失的剂量为1.75克/千克/天的第三个孕孕孕级酒精暴露，母亲和胎儿肾上腺皮质激素（ACTH）和皮质醇水平升高响应酒精治疗。在这项研究中，我们假设来自慢性静脉醇的皮质醇中的重复升高至少部分地负责胎儿神经元缺陷。将动物分为四组：正常对照，对喂养的盐水控制，醇和皮质醇。通过在实验的每天用氢化可血液用氢化态造成6小时，在皮质菌中造成醇的升高，在皮质醇组中模仿，在实验的每一天中，在第一小时内给予盐水以代替酒精。该实验在连续三天进行，然后在妊娠日（GD）109开始的情况下进行4天，直至GD 132.醇组中的母体血液醇浓度为239±7mg / dl。收集胎儿大脑并加工在GD 133上计数的立体电池。胎儿小脑尿布内细胞的估计总数，参考体积和尿红杂交细胞密度响应于糖皮质激素在没有醇的情况下不改变。这些结果表明，糖皮质激素在第三个三个月的当量期间独立地产生胎儿小脑缺乏细胞损失。然而，皮质醇的升高以及酒精诱导的其他变化可以一起导致胎儿酒精谱系疾病中看到的脑损伤。

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  • 来源
    《Alcohol》 |2013年第1期|共9页
  • 作者

    WashburnS.E.; TressU.; LundeE.R.; ChenW.J.A.; CuddT.A.;

  • 作者单位

    Department of Veterinary Physiology and Pharmacology and Michael E. DeBakey Institute College of;

    Laboklin GmbH Veterinary Laboratory Diagnostic Steubenstr. 7 97688 Bad Kissingen Germany;

    Department of Veterinary Physiology and Pharmacology and Michael E. DeBakey Institute College of;

    Department of Neuroscience and Experimental Therapeutics Texas A and M Health Science Center;

    Department of Veterinary Physiology and Pharmacology and Michael E. DeBakey Institute College of;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 中毒及化学性损害;
  • 关键词

    Cerebellum; Cortisol; Ethanol; Fetal alcohol spectrum disorder; Fetal alcohol syndrome; Sheep;

    机译：小脑;皮质醇;乙醇;胎儿酒精谱系障碍;胎儿酒精综合征;羊;

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