...
首页> 外文期刊>Ecotoxicology and Environmental Safety >Prenatal exposure to diesel exhaust particles causes anxiety, spatial memory disorders with alters expression of hippocampal pro-inflammatory cytokines and NMDA receptor subunits in adult male mice offspring
【24h】

Prenatal exposure to diesel exhaust particles causes anxiety, spatial memory disorders with alters expression of hippocampal pro-inflammatory cytokines and NMDA receptor subunits in adult male mice offspring

机译:柴油排气颗粒的产前暴露导致焦虑,空间记忆障碍与大型雄性小鼠后代的海马促炎细胞因子和NMDA受体亚基的改变表达

获取原文
获取原文并翻译 | 示例
           

摘要

Air pollution by Diesel exhaust (DE) consists of gaseous compounds and diesel exhaust particles (DEPs). Previous studies show associations between prenatal exposure to diesel exhaust affects the central nervous system (CNS). However, there was not reported that these effects were caused by gaseous compounds, diesel exhaust particles, or both. A limited number of studies in rodent models have shown that exposure to DEPs can result in CNS. Here, we explored the effects of prenatal exposure to DEPs on anxiety and learning and memory in NMRI mice male offspring.Three groups of pregnant mice were exposed to 350-400 mu g DEPs/m(3) for 2, 4 and 6 h daily in a closed system room. We examined anxiety and learning and memory in 8-to-9-week-old male offspring using the Elevated plus maze and Morris water maze (MWM) test. Hippocampi were isolated after the behavioral tests and measured pro-inflammatory cytokines and N-methyl-D-aspartate (NMDA) receptor expression by quantitative RT-PCR analysis. Mice exposed to DEPs in utero showed deficits in the Elevated plus maze and Morris water maze test. In addition, DEPs exposed mice exhibited decreased hippocampal NR2A and NR3B expression. Taken together, our data suggest that maternal DEP exposure is associated with anxiety, disrupts learning and memory and reduction hippocampal NR2A and NR3B expression in male offspring.
机译:柴油排气(DE)的空气污染由气态化合物和柴油排气颗粒(DEPS)组成。以前的研究表明产前暴露于柴油排气之间的关联会影响中枢神经系统(CNS)。然而,没有报道这些效应是由气态化合物,柴油排气颗粒或两者引起的。啮齿动物模型的有限数量的研究表明,暴露于DEPS可能导致CNS。在这里,我们探讨了产前暴露于DEPS对NMRI小鼠男性后代的焦虑和学习和记忆的影响。每天暴露于350-400 mu G DEPS / M(3)的三组,每日2,4和6小时在一个封闭的系统室内。我们在使用升高的加迷宫和莫里斯水迷宫(MWM)测试中,在8至9周龄男性后代检查了焦虑和学习和记忆。通过定量RT-PCR分析在行为试验和测量的促炎细胞因子和N-甲基-D-天冬氨酸(NMDA)受体表达后分离出海马。暴露于Uttero的Deps的小鼠在升高的加迷宫和Morris水迷宫测试中显示出缺陷。此外,DEPS暴露的小鼠表现出降低的海马NR2a和NR3b表达。我们的数据结合在一起,表明母体Dep曝光与焦虑有关,扰乱了雄性后代中的学习和记忆和降低海马NR2A和NR3B表达。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号