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

Kiyokazu Ogita, Masanori Yoneyama, Shigeru Hasebe, Tatsuo Shiba
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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.

[激活的小胶质细胞在成年小鼠齿状回神经元丢失后触发神经发生]。
众所周知,神经损伤可促进成年海马齿状回的神经发生。我们前期的研究表明,海马齿状回颗粒细胞在三甲基锡(TMT)的作用下被损伤和根除,并在神经元丢失后在齿状颗粒细胞层(GCL)再生。最近的集体报道表明,在脑损伤和神经退行性疾病中,神经发生受细胞因子、趋化因子、神经递质和活性氧/氮物质的控制,这些物质由死亡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。为了阐明激活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,本研究评估了激活的小胶质细胞及其相关因子在TMT诱导的海马齿状回神经元丢失后新生细胞生成中的作用。我们的研究结果支持了一种可能性,即激活的小胶质细胞释放的促炎细胞因子可能通过激活NF-kappaB信号通路参与了TMT治疗诱导的齿状神经元丢失后神经发生机制的促进。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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