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Microglial contributions to aberrant neurogenesis and pathophysiology of epilepsy

Microglia are dynamic cells that constitute the brain’s innate immune system. Recently, research has demonstrated microglial roles beyond immunity, which include homeostatic roles in the central nervous system. The function of microglia is an active area of study, with insights into changes in neuro...

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Detalles Bibliográficos
Autores principales: Victor, Tanya R., Tsirka, Stella E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7641338/
https://www.ncbi.nlm.nih.gov/pubmed/33154976
http://dx.doi.org/10.20517/2347-8659.2020.02
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author Victor, Tanya R.
Tsirka, Stella E.
author_facet Victor, Tanya R.
Tsirka, Stella E.
author_sort Victor, Tanya R.
collection PubMed
description Microglia are dynamic cells that constitute the brain’s innate immune system. Recently, research has demonstrated microglial roles beyond immunity, which include homeostatic roles in the central nervous system. The function of microglia is an active area of study, with insights into changes in neurogenesis and synaptic pruning being discovered in both health and disease. In epilepsy, activated microglia contribute to several changes that occur during epileptogenesis. In this review, we focus on the effects of microglia on neurogenesis and synaptic pruning, and discuss the current state of anti-seizure drugs and how they affect microglia during these processes. Our understanding of the role of microglia post-seizure is still limited and may be pivotal in recognizing new therapeutic targets for seizure intervention.
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spelling pubmed-76413382020-11-04 Microglial contributions to aberrant neurogenesis and pathophysiology of epilepsy Victor, Tanya R. Tsirka, Stella E. Neuroimmunol Neuroinflamm Article Microglia are dynamic cells that constitute the brain’s innate immune system. Recently, research has demonstrated microglial roles beyond immunity, which include homeostatic roles in the central nervous system. The function of microglia is an active area of study, with insights into changes in neurogenesis and synaptic pruning being discovered in both health and disease. In epilepsy, activated microglia contribute to several changes that occur during epileptogenesis. In this review, we focus on the effects of microglia on neurogenesis and synaptic pruning, and discuss the current state of anti-seizure drugs and how they affect microglia during these processes. Our understanding of the role of microglia post-seizure is still limited and may be pivotal in recognizing new therapeutic targets for seizure intervention. 2020-07-12 2020 /pmc/articles/PMC7641338/ /pubmed/33154976 http://dx.doi.org/10.20517/2347-8659.2020.02 Text en Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Article
Victor, Tanya R.
Tsirka, Stella E.
Microglial contributions to aberrant neurogenesis and pathophysiology of epilepsy
title Microglial contributions to aberrant neurogenesis and pathophysiology of epilepsy
title_full Microglial contributions to aberrant neurogenesis and pathophysiology of epilepsy
title_fullStr Microglial contributions to aberrant neurogenesis and pathophysiology of epilepsy
title_full_unstemmed Microglial contributions to aberrant neurogenesis and pathophysiology of epilepsy
title_short Microglial contributions to aberrant neurogenesis and pathophysiology of epilepsy
title_sort microglial contributions to aberrant neurogenesis and pathophysiology of epilepsy
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7641338/
https://www.ncbi.nlm.nih.gov/pubmed/33154976
http://dx.doi.org/10.20517/2347-8659.2020.02
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