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[成年小鼠齿状回神经元丢失后,活化的小胶质细胞触发神经发生]

[Activated microglial cells trigger neurogenesis following neuronal loss in the dentate gyrus of adult mice].

作者信息

Ogita Kiyokazu, Yoneyama Masanori, Hasebe Shigeru, Shiba Tatsuo

机构信息

Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University, 45-1, Nagaotoge-cho, Hirakata 573-0101, Japan.

出版信息

Nihon Shinkei Seishin Yakurigaku Zasshi. 2012 Nov;32(5-6):281-5.

Abstract

Neurological injuries are widely known to promote neurogenesis in the adult hippocampal dentate gyrus. Our previous studies demonstrated that the granule cells in the hippocampal dentate gyrus are injured and eradicated by treatment with trimethyltin (TMT), with being regenerated in the dentate granule cell layer (GCL) after neuronal loss. Recent collective reports indicate that during brain injury and in neurodegenerative disorders, neurogenesis is controlled by cytokines, chemokines, neurotransmitters, and reactive oxygen/nitrogen species, which are released by dying neurons as well as by activated macrophages, micro-glia, and astrocytes. To elucidate the role of activated microglia in the neuroregeneration following the dentate granule cell loss, in this study, we evaluated the involvement of activated microglial cells and a related factor in the generation of newly-generated cells of the hippocampal dentate gyrus following neuronal loss induced by TMT. Our results support the possibility that pro-inflammatory cytokines released from activated microglial cells may be involved in promotion of the neurogenesis mechanism through activation of the NF-kappaB signaling pathway following the dentate neuronal loss induced by TMT treatment.

摘要

众所周知,神经损伤可促进成年海马齿状回中的神经发生。我们之前的研究表明,用三甲基锡(TMT)处理会损伤并消除海马齿状回中的颗粒细胞,神经元丢失后齿状颗粒细胞层(GCL)会再生。最近的综合报道表明,在脑损伤和神经退行性疾病期间,神经发生受细胞因子、趋化因子、神经递质以及活性氧/氮物质的控制,这些物质由垂死的神经元以及活化的巨噬细胞、小胶质细胞和星形胶质细胞释放。为了阐明活化的小胶质细胞在齿状颗粒细胞丢失后的神经再生中的作用,在本研究中,我们评估了活化的小胶质细胞和相关因子在TMT诱导神经元丢失后海马齿状回新生细胞生成中的作用。我们的结果支持这样一种可能性,即活化的小胶质细胞释放的促炎细胞因子可能通过TMT处理诱导的齿状神经元丢失后激活NF-κB信号通路参与促进神经发生机制。

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