Prenatal exposure to ethanol causes differential effects in nerve growth factor and its receptor in the basal forebrain of preweaning and adult rats
Prenatal exposure to ethanol causes differential effects in nerve growth factor and its receptor in the basal forebrain of preweaning and adult rats
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DOI：
10.1155/np.1997.63
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发表时间：
1997-04-01
期刊：
影响因子：
--
通讯作者：
Aloe, L
中科院分区：
文献类型：
--
作者：
Angelucci, F;Cimino, M;Aloe, L
在这项研究中，我们研究了在妊娠第 15 天接受单次胃内急性乙醇注射的怀孕雌性 Sprague-Dawley 大鼠的后代皮质和海马中神经生长因子 (NGF) 的水平，并将其与注射蔗糖的对照组大鼠进行比较。我们还检查了低亲和力 NGF 受体 p75NGFR 在位于 Meynert 隔膜和核中的 NGF 响应神经元上的分布，这些神经元分别接受来自海马和皮质的营养支持。在乙醇治疗组中，结果显示在出生后15天时，NGF隔海马通路受到显着影响。第 15 天，乙醇处理的大鼠后代的 NGF 水平显着升高。到第 40 天，两组的 NGF 值均降至相似水平。然而，在第 60 天，乙醇治疗组动物的 NGF 水平明显低于对照组，但基本保持不变。与此同时，在第 60 天，乙醇处理的大鼠中表达 p75NGFR 的间隔胆碱能神经元的数量也显着低于对照动物。由于已知乙醇会诱发神经系统疾病以及细胞增殖和分化缺陷，因此研究结果表明，乙醇引起有害影响的原因之一是在出生后大脑发育的某些阶段 NGF 的可用性较低。
In this study we investigated nerve growth factor (NGF) levels in the cortex and hippocampus of the offspring of pregnant female Sprague-Dawley rats receiving a single intragastric administration of acute ethanol on the 15th day of gestation and compared them with a control group of rats that received an injection of sucrose. We also examined the distribution of the low-affinity NGF receptor, p75NGFR, on NGF-responsive neurons that are localized in the septum and the nucleus of Meynert, which receive the respective trophic support from the hippocampus and the cortex. In the ethanol-treated group, the results show that at post-natal age 15 days, the NGF septohippocampal pathways were markedly affected. At day 15, the NGF level was significantly higher in the offspring of ethanol-treated rats. By day 40, NGF values in both groups decreased to similar levels. At day 60, however, the NGF level in the ethanol-treated animals decreased to a significantly lower value than that of the control group, which remained essentially unchanged. In parallel, at day 60 the numbers of septal cholinergic neurons expressing p75NGFR were also significantly lower in ethanol-treated rats than in control animals. Because ethanol is known to induce neurological disorders, as well as deficits in cell proliferation and differentiation, the results suggest that one cause of the deleterious effects induced by ethanol is the low availability of NGF during certain stages of postnatal brain development.