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光生物调节调节癫痫动物模型中海马中的成年神经发生。

Photobiomodulation regulates adult neurogenesis in the hippocampus in a status epilepticus animal model.

机构信息

Medical Laser Research Center, Dankook University, Cheonan, Republic of Korea.

Department of Biomedical Science, College of Medicine, Dankook University, Cheonan, Republic of Korea.

出版信息

Sci Rep. 2022 Sep 9;12(1):15246. doi: 10.1038/s41598-022-19607-5.

Abstract

Status epilepticus (SE) refers to a single seizure that lasts longer than typical seizures or a series of consecutive seizures. The hippocampus, which is vulnerable to the effects of SE, has a critical role in memory storage and retrieval. The trisynaptic loop in the hippocampus connects the substructures thereof, namely the dentate gyrus (DG), CA3, and CA1. In an animal model of SE, abnormal neurogenesis in the DG and aberrant neural network formation result in sequential neural degeneration in CA3 and CA1. Photobiomodulation (PBM) therapy, previously known as low-level laser (light) therapy (LLLT), is a novel therapy for the treatment of various neurological disorders including SE. However, the effects of this novel therapeutic approach on the recovery process are poorly understood. In the present study, we found that PBM transformed SE-induced abnormal neurogenesis to normal neurogenesis. We demonstrated that PBM plays a key role in normal hippocampal neurogenesis by enhancing the migration of maturing granular cells (early neuronal cells) to the GCL, and that normal neurogenesis induced by PBM prevents SE-induced hippocampal neuronal loss in CA1. Thus, PBM is a novel approach to prevent seizure-induced neuronal degeneration, for which light devices may be developed in the future.

摘要

癫痫持续状态(SE)是指单次发作持续时间长于典型发作或一系列连续发作。海马体易受 SE 的影响,在记忆存储和检索中起着关键作用。海马体的三突触环连接其亚结构,即齿状回(DG)、CA3 和 CA1。在 SE 的动物模型中,DG 中的异常神经发生和异常神经网络形成导致 CA3 和 CA1 中的顺序神经变性。光生物调节(PBM)疗法,以前称为低水平激光(光)疗法(LLLT),是一种治疗各种神经障碍的新疗法,包括 SE。然而,这种新的治疗方法对恢复过程的影响知之甚少。在本研究中,我们发现 PBM 将 SE 诱导的异常神经发生转化为正常神经发生。我们证明 PBM 通过增强成熟颗粒细胞(早期神经元细胞)向 GCL 的迁移来发挥关键作用,并且 PBM 诱导的正常神经发生可防止 SE 诱导的 CA1 中海马神经元丢失。因此,PBM 是一种预防癫痫发作诱导的神经元退化的新方法,未来可能会开发出光设备。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27b2/9463127/54adb59d53c1/41598_2022_19607_Fig1_HTML.jpg

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