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产前应激通过谷氨酸导致仔鼠海马 CA3 区锥体神经元树突萎缩。

Prenatal stress causes dendritic atrophy of pyramidal neurons in hippocampal CA3 region by glutamate in offspring rats.

机构信息

Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, People's Republic of China.

出版信息

Dev Neurobiol. 2010 Feb;70(2):114-25. doi: 10.1002/dneu.20766.

DOI:10.1002/dneu.20766
PMID:19950194
Abstract

A substantial number of human epidemiological data, as well as experimental studies, suggest that adverse maternal stress during gestation is involved in abnormal behavior, mental, and cognition disorder in offspring. To explore the effect of prenatal stress (PS) on hippocampal neurons, in this study, we observed the dendritic field of pyramidal neurons in hippocampal CA3, examined the concentration of glutamate (Glu), and detected the expression of synaptotagmin-1 (Syt-1) and N-methyl-D-aspartate receptor 1 (NR1) in hippocampus of juvenile female offspring rats. Pregnant rats were divided into two groups: control group (CON) and PS group. Female offspring rats used were 30-day old. The total length of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly shorter in PS than that in CON (p < 0.01). The number of branch points of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly less in PS (p < 0.01). PS offspring had a higher concentration of hippocampal Glu compared with CON (p < 0.05). PS offspring displayed increased expression of Syt-1 and decreased NR1 in hippocampus compared with CON (p < 0.001 and p < 0.01, respectively). The expression of NR1 in different hippocampus subfields of offspring was significantly decreased in PS than that in CON (p < 0.05-0.01). This study shows that PS increases the Glu in hippocampus and causes apical dendritic atrophy of pyramidal neurons of hippocampal CA3 in offspring rats. The decline of NR1 in hippocampus may be an adaptive response to the increased Glu.

摘要

大量的人类流行病学数据以及实验研究表明,妊娠期间母体的不良应激与后代的异常行为、精神和认知障碍有关。为了探讨产前应激(PS)对海马神经元的影响,本研究观察了海马 CA3 区锥体神经元的树突野,检测了海马谷氨酸(Glu)浓度,并检测了海马突触结合蛋白-1(Syt-1)和 N-甲基-D-天冬氨酸受体 1(NR1)的表达。将怀孕大鼠分为两组:对照组(CON)和 PS 组。雌性后代大鼠为 30 日龄。PS 组的海马 CA3 区锥体神经元顶树突总长度明显短于 CON 组(p < 0.01)。PS 组海马 CA3 区锥体神经元顶树突的分支点数量明显少于 CON 组(p < 0.01)。PS 组的海马 Glu 浓度明显高于 CON 组(p < 0.05)。PS 组的海马 Syt-1 表达增加,NR1 表达减少,与 CON 组相比差异有统计学意义(p < 0.001 和 p < 0.01)。PS 组的海马不同脑区 NR1 的表达明显低于 CON 组(p < 0.05-0.01)。本研究表明,PS 增加了海马 Glu,并导致后代大鼠海马 CA3 区锥体神经元的顶树突萎缩。海马 NR1 的下降可能是对 Glu 增加的适应性反应。

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