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Photobiomodulation regulates adult neurogenesis in the hippocampus in a status epilepticus animal model
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 substru...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9463127/ https://www.ncbi.nlm.nih.gov/pubmed/36085308 http://dx.doi.org/10.1038/s41598-022-19607-5 |
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author | Hong, Namgue Kang, Gi Won Park, Ji On Chung, Phil-Sang Lee, Min Young Ahn, Jin-Chul |
author_facet | Hong, Namgue Kang, Gi Won Park, Ji On Chung, Phil-Sang Lee, Min Young Ahn, Jin-Chul |
author_sort | Hong, Namgue |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9463127 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-94631272022-09-11 Photobiomodulation regulates adult neurogenesis in the hippocampus in a status epilepticus animal model Hong, Namgue Kang, Gi Won Park, Ji On Chung, Phil-Sang Lee, Min Young Ahn, Jin-Chul Sci Rep Article 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. Nature Publishing Group UK 2022-09-09 /pmc/articles/PMC9463127/ /pubmed/36085308 http://dx.doi.org/10.1038/s41598-022-19607-5 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Hong, Namgue Kang, Gi Won Park, Ji On Chung, Phil-Sang Lee, Min Young Ahn, Jin-Chul Photobiomodulation regulates adult neurogenesis in the hippocampus in a status epilepticus animal model |
title | Photobiomodulation regulates adult neurogenesis in the hippocampus in a status epilepticus animal model |
title_full | Photobiomodulation regulates adult neurogenesis in the hippocampus in a status epilepticus animal model |
title_fullStr | Photobiomodulation regulates adult neurogenesis in the hippocampus in a status epilepticus animal model |
title_full_unstemmed | Photobiomodulation regulates adult neurogenesis in the hippocampus in a status epilepticus animal model |
title_short | Photobiomodulation regulates adult neurogenesis in the hippocampus in a status epilepticus animal model |
title_sort | photobiomodulation regulates adult neurogenesis in the hippocampus in a status epilepticus animal model |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9463127/ https://www.ncbi.nlm.nih.gov/pubmed/36085308 http://dx.doi.org/10.1038/s41598-022-19607-5 |
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