Hippocampal cell proliferation is reduced following prenatal ethanol exposure but can be rescued with voluntary exercise
Hippocampal cell proliferation is reduced following prenatal ethanol exposure but can be rescued with voluntary exercise
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DOI：
10.1002/hipo.20164
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发表时间：
2006-01-01
期刊：
影响因子：
3.5
通讯作者：
Christie, BR
中科院分区：
文献类型：
--
作者：
Redila, VA;Olson, AK;Christie, BR
怀孕期间摄入乙醇会对未出生的后代产生许多有害后果，产生结构和功能缺陷，影响大脑和许多其他器官直至成年。海马体是对乙醇的副作用特别敏感的大脑区域。在之前的一项研究中，我们表明，自愿锻炼可以改善产前乙醇暴露后发生的长期增强和行为缺陷（Eur J Neurosci，2005，21，1719-1726）。在本研究中，我们研究了产前乙醇暴露对成年期神经发生的影响，并检验了自愿锻炼可以改善观察到的任何缺陷的假设。 Sprague-Dawley 雌性在整个妊娠期间接受三种饮食之一：0) 乙醇 (E)，一种含有 36.5% 乙醇衍生热量的液体饮食； (ii) 配对喂养 (PF)，一种液体对照饮食，用麦芽糖糊精等热量替代乙醇，其摄入量为 E 伴侣的消耗量（克/千克体重/妊娠天）； (iii)随意饲喂对照(C)，正常实验室饲料和水，随意。后代在出生后第 35 天（PND）被单独饲养，并在 PND 50 时被随机分配到有或没有运动轮的笼子里。在 PND 57 时注射 BrdU（200 mg/kg，IP），动物在 24 小时（增殖）或 4 周（神经发生）后终止。我们的结果表明，产前乙醇暴露显着降低了成年齿状回的细胞增殖和神经发生。处于 PF 状态的动物也表现出神经发生减少。相比之下，所有参与自愿运动的动物的细胞增殖和神经发生均显着增加。这些结果表明，产前乙醇暴露可以抑制细胞增殖和神经发生，并且这些影响可能至少部分是由营养介导的。重要的是，自愿运动似乎对在子宫内接触乙醇的动物中观察到的海马体积和细胞数量的长期缺陷有有益的影响。 (c) 2006 Wiley-Liss, Inc.
The ingestion of ethanol during pregnancy has a number of deleterious consequences for the unborn offspring, producing structural and functional deficits that affect the brain and many other organs into adulthood. The hippocampus is a brain area that is particularly sensitive to ethanol's adverse effects. In a previous study we showed that voluntary exercise can ameliorate deficits in long-term potentiation and behavior that occur following prenatal ethanol exposure (Eur J Neurosci, 2005, 21, 1719-1726). In the present study, we investigated the effects of prenatal ethanol exposure on neurogenesis in adulthood, and tested the hypothesis that voluntary exercise would ameliorate any deficits observed. Sprague-Dawley females were administered one of three diets throughout gestation: 0) ethanol (E), a liquid diet containing 36.5% ethanol-derived calories; (ii) pair-fed (PF), a liquid control diet, with maltose-dextrin isocalorically substituted for ethanol, in the amount consumed by an E partner (g/kg body wt/day of gestation); and (iii) ad-libitum-fed control (C), normal laboratory chow and water, ad libitum. The offspring were housed individually at postnatal day (PND) 35, and at PND 50 were randomly assigned to cages either with or without an exercise wheel. BrdU (200 mg/kg, I.P.) was injected on PND 57, and animals terminated either 24 h (proliferation) or 4 weeks (neurogenesis) later. Our results demonstrate that prenatal ethanol exposure significantly decreases both cell proliferation and neurogenesis in the adult dentate gyrus. Animals in the PF condition also showed reduced neurogenesis. in contrast, all animals that engaged in voluntary exercise showed a significant increase in cell proliferation and neurogenesis. These results indicate that prenatal ethanol exposure can suppress both cell proliferation and neurogenesis, and that these effects may be, at least in part, nutritionally mediated. Importantly, voluntary exercise appears to have beneficial effects for these long-lasting deficits in hippocampal volume and cell number that have been observed in animals exposed to ethanol in utero. (c) 2006 Wiley-Liss, Inc.