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产前应激子代海马中细胞外信号调节激酶(ERK)表达的性别和区域差异。

Sex and region difference of the expression of ERK in prenatal stress offspring hippocampus.

作者信息

Cai Qing, Zhu Zhongliang, Huang Shuyun, Li Hui, Fan Xiaoli, Jia Ning, Zhang Boli, Song Liang, Li Qinghong, Liu Jiankang

机构信息

Tianjin University of Traditional Medicine, Tianjin 300193, PR China.

出版信息

Int J Dev Neurosci. 2007 Jun;25(4):207-13. doi: 10.1016/j.ijdevneu.2007.03.009. Epub 2007 Apr 3.

Abstract

Prenatal stress is known to cause neuronal loss and oxidative damage in the hippocampus of offspring rats. The underlying molecular mechanism has not been fully understood. The extracellularsignal-regulated kinase (ERK1/2) is recruited when the brain undergoes synaptic plasticity and remodeling. In the present study, we used Western blotting and immunohistochemistry techniques to examine the effects of prenatal restraint stress (PNS) on the expression of phosphorylated ERK (p-ERK) and total ERK. Pregnant rats in the PNS group were exposed to restraint stress on day 14-20 of pregnancy three times daily for 45min. One-month-old offspring rats were used in this experiment. PNS treatment increased the expression of p-ERK2 compared to that in the control female offspring rats and total ERK2 in female offspring hippocampus compared with that of control group. No significant changes in the amounts of total ERK1 of prenatally offspring hippocampus were observed in both genders compared with control animals. ERK immunodensity was significantly increased in PNS groups in CA3 field in male offspring hippocampus compared with control animals. ERK optical density was significantly increased in PNS female offspring hippocampus CA1, CA3 and CA4 region. However, ERK optical density was not significantly different between male control and PNS groups in CA1, CA4 fields and DG in offspring hippocampus. These findings suggest the sex and region-dependent effects of prenatal stress on the expression of ERK in offspring hippocampus. ERK expression changes induced by prenatal stress may contribute to hippocampus synaptic plasticity changes of the offspring.

摘要

已知产前应激会导致子代大鼠海马体中的神经元丢失和氧化损伤。其潜在的分子机制尚未完全明确。当大脑经历突触可塑性和重塑时,细胞外信号调节激酶(ERK1/2)会被激活。在本研究中,我们使用蛋白质免疫印迹法和免疫组织化学技术来检测产前束缚应激(PNS)对磷酸化ERK(p-ERK)和总ERK表达的影响。PNS组的怀孕大鼠在妊娠第14至20天每天接受3次束缚应激,每次45分钟。本实验使用1月龄的子代大鼠。与对照雌性子代大鼠相比,PNS处理增加了雌性子代海马体中p-ERK2的表达,与对照组相比,雌性子代海马体中总ERK2的表达也增加。与对照动物相比,在两种性别中,产前子代海马体中总ERK1的量均未观察到显著变化。与对照动物相比,雄性子代海马体CA3区PNS组的ERK免疫密度显著增加。PNS雌性子代海马体CA1、CA3和CA4区的ERK光密度显著增加。然而,在子代海马体的CA1、CA4区和齿状回中,雄性对照和PNS组之间的ERK光密度没有显著差异。这些发现表明产前应激对子代海马体中ERK表达具有性别和区域依赖性影响。产前应激诱导的ERK表达变化可能有助于子代海马体突触可塑性的改变。

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