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匹罗卡品诱导癫痫持续状态小鼠中,强制体力训练增加神经元增殖和成熟,并使其整合到正常回路中。

Forced Physical Training Increases Neuronal Proliferation and Maturation with Their Integration into Normal Circuits in Pilocarpine Induced Status Epilepticus Mice.

机构信息

Institute of Neurobiology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an, 710061, China.

Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an, 710061, China.

出版信息

Neurochem Res. 2019 Nov;44(11):2590-2605. doi: 10.1007/s11064-019-02877-3. Epub 2019 Sep 27.

Abstract

Increased number of newly-born neurons produced at latent stage after status epilepticus (SE) contribute to aberrant rewiring of hippocampus and are hypothesized to promote epileptogenesis. Although physical training (PT) was reported to cause further increase in neurogenesis after SE, how PT affect their integration pattern is still elusive, whether they integrate into normal circuits or increase aberrant integrations is yet to be determined. To understand this basic mechanism by which PT effects SE and to elaborate the possible role of neuronal integrations in prognosis of SE, we evaluated the effect of 4 weeks of treadmill PT in adult male mice after pilocarpine-induced SE on behavioral and aberrant integrations' parameters. Changes in BDNF gene methylation and its protein level in hippocampus was also measured at latent stage (2-weeks) to explore underlying pathways involved in increasing neurogenesis. Our results demonstrated that although PT increased proliferation and maturation of neurons in dentate gyrus, they showed reduced aberrant integrations into hippocampal circuitry assessed through a decrease in the number of ectopic granular cells, hilar basal dendrites and mossy fiber sprouting as compared to non-exercised SE mice. While SE decreased the percentage methylation of specific CpGs of BDNF gene's promoter, PT did not yield any significant difference in methylation of BDNF CpGs as compared to non-exercised SE mice. In conclusion, PT increases hippocampal neurogenesis through increasing BDNF levels by some pathways other than demethylating BDNF CpGs and causes post SE newly-born neurons to integrate into normal circuits thus resulting in decreased spontaneous recurrent seizures and enhanced spatial memory.

摘要

癫痫持续状态(SE)后潜伏期新生神经元数量增加导致海马异常重连,并被假设促进癫痫发生。尽管有报道称,运动训练(PT)会在 SE 后进一步增加神经发生,但 PT 如何影响其整合模式仍不清楚,它们是整合到正常回路中还是增加异常整合仍有待确定。为了了解 PT 对 SE 的影响的基本机制,并详细阐述神经元整合在 SE 预后中的可能作用,我们评估了成年雄性小鼠在匹罗卡品诱导的 SE 后 4 周跑步机 PT 对行为和异常整合参数的影响。还在潜伏期(2 周)测量海马 BDNF 基因甲基化及其蛋白水平的变化,以探索参与增加神经发生的潜在途径。我们的结果表明,尽管 PT 增加了齿状回神经元的增殖和成熟,但与未进行 PT 的 SE 小鼠相比,它们进入海马回路的异常整合减少,表现为异位颗粒细胞、门区基底树突和苔藓纤维发芽的数量减少。虽然 SE 降低了 BDNF 基因启动子特定 CpG 的甲基化百分比,但与未进行 PT 的 SE 小鼠相比,PT 对 BDNF CpG 的甲基化没有产生任何显著差异。总之,PT 通过增加 BDNF 水平增加海马神经发生,而不是通过去甲基化 BDNF CpGs 的某些途径,导致 SE 后新生神经元整合到正常回路中,从而减少自发性反复性癫痫发作并增强空间记忆。

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