首页> 外文期刊>Neurotoxicology >Increased hippocampal mRNA expression of neuronal synaptic plasticity related genes in mice chronically exposed to toluene at a low-level human occupational-exposure.
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Increased hippocampal mRNA expression of neuronal synaptic plasticity related genes in mice chronically exposed to toluene at a low-level human occupational-exposure.

机译:在低水平人类职业暴露下长期暴露于甲苯的小鼠中,神经元突触可塑性相关基因的海马mRNA表达增加。

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摘要

Although neurological symptoms in individuals exposed to toluene both inside and outside the homes have been reported well, the chronic effects of low-level toluene-exposure on the hippocampal expression of neuronal synaptic plasticity related genes have not been studied in vivo. In the present study, to understand the possible adult hippocampal neurobiological responses of mice chronic exposure to toluene at a low-level human occupational-exposure, we exposed 10-week-old C3H/HeN female mice to 50 ppm toluene or filtered air for 6 h a day, on 5-consecutive days of a week for 6 and 12 weeks, in a whole-body exposure chamber. Then, by a quantitative real-time PCR method, we investigated the hippocampal mRNA-expression of several genes, functions of which are necessary to maintain the homeostasis of neuronal synaptic plasticity. We observed that chronic exposure of mice to 50 ppm toluene for a longer period (12 weeks) caused a significant up-regulation of NMDA receptor subunit 2B (NMDA NR2B) expression associated with a simultaneous induction of CaMKIV, CREB-1, and FosB/DeltaFosB in the same hippocampal tissues. Our data indicate that the in vivo transcriptional up-regulation of these genes in the adult hippocampus of our experimental mouse model following the chronic exposure to toluene may be an NMDA-receptor related neuroprotective mechanism of gene expression.
机译:尽管在家庭内部和外部都暴露于甲苯的个体的神经系统症状已有很好的报道,但体内低水平甲苯暴露对神经元突触可塑性相关基因海马表达的慢性影响尚未得到研究。在本研究中,为了了解在低水平人类职业暴露下长期暴露于甲苯的小鼠可能产生的成年海马神经生物学反应,我们将10周龄的C3H / HeN雌性小鼠暴露于50 ppm甲苯或过滤空气中6在全身暴露室内,连续一周连续5天,连续6天和12周,每天每公顷。然后,通过实时定量PCR方法,我们调查了几个基因的海马mRNA表达,其功能对于维持神经元突触可塑性的稳态是必不可少的。我们观察到,小鼠长期暴露于50 ppm甲苯的时间较长(12周)会导致NMDA受体亚基2B(NMDA NR2B)的表达明显上调,同时诱导CaMKIV,CREB-1和FosB / DeltaFosB位于相同的海马组织中。我们的数据表明,在长期暴露于甲苯后,我们实验小鼠模型的成年海马中这些基因的体内转录上调可能是基因表达与NMDA受体相关的神经保护机制。

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