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Contributions of Microglia to Structural Synaptic Plasticity

Synaptic plasticity critically depends on reciprocal interactions between neurons and glia. Among glial cells, microglia represent approximately 10% of the total brain cell population serve as the brain’s resident macrophage, and help to modulate neural activity. Because of their special role in the...

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Detalles Bibliográficos
Autores principales: Kim, Kyung Ho, Son, Sung Min, Mook-Jung, Inhee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Libertas Academica 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4089681/
https://www.ncbi.nlm.nih.gov/pubmed/25157211
http://dx.doi.org/10.4137/JEN.S11269
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author Kim, Kyung Ho
Son, Sung Min
Mook-Jung, Inhee
author_facet Kim, Kyung Ho
Son, Sung Min
Mook-Jung, Inhee
author_sort Kim, Kyung Ho
collection PubMed
description Synaptic plasticity critically depends on reciprocal interactions between neurons and glia. Among glial cells, microglia represent approximately 10% of the total brain cell population serve as the brain’s resident macrophage, and help to modulate neural activity. Because of their special role in the brain’s immune response, microglia are involved in the pathological progression of neurodegenerative disorders such as Alzheimer’s disease (AD). However, microglia also are surveyors of the brain’s health and continuously contact dendritic spines to regulate structural synaptic changes. This review summarizes our current understanding of neuronal-microglial signals that affect neural function at the synapse. Here, we examine the role of microglia in neuronal synapses in pathological brains and specifically focus on in vivo studies using 2-photon microscopy. Furthermore, because the role of microglia in AD progression is controversial, we outline the interaction between neurons and microglia in pathological conditions such as AD.
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spelling pubmed-40896812014-08-25 Contributions of Microglia to Structural Synaptic Plasticity Kim, Kyung Ho Son, Sung Min Mook-Jung, Inhee J Exp Neurosci Review Synaptic plasticity critically depends on reciprocal interactions between neurons and glia. Among glial cells, microglia represent approximately 10% of the total brain cell population serve as the brain’s resident macrophage, and help to modulate neural activity. Because of their special role in the brain’s immune response, microglia are involved in the pathological progression of neurodegenerative disorders such as Alzheimer’s disease (AD). However, microglia also are surveyors of the brain’s health and continuously contact dendritic spines to regulate structural synaptic changes. This review summarizes our current understanding of neuronal-microglial signals that affect neural function at the synapse. Here, we examine the role of microglia in neuronal synapses in pathological brains and specifically focus on in vivo studies using 2-photon microscopy. Furthermore, because the role of microglia in AD progression is controversial, we outline the interaction between neurons and microglia in pathological conditions such as AD. Libertas Academica 2013-10-31 /pmc/articles/PMC4089681/ /pubmed/25157211 http://dx.doi.org/10.4137/JEN.S11269 Text en © 2013 the author(s), publisher and licensee Libertas Academica Ltd. This is an open access article published under the Creative Commons CC-BY-NC 3.0 license.
spellingShingle Review
Kim, Kyung Ho
Son, Sung Min
Mook-Jung, Inhee
Contributions of Microglia to Structural Synaptic Plasticity
title Contributions of Microglia to Structural Synaptic Plasticity
title_full Contributions of Microglia to Structural Synaptic Plasticity
title_fullStr Contributions of Microglia to Structural Synaptic Plasticity
title_full_unstemmed Contributions of Microglia to Structural Synaptic Plasticity
title_short Contributions of Microglia to Structural Synaptic Plasticity
title_sort contributions of microglia to structural synaptic plasticity
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4089681/
https://www.ncbi.nlm.nih.gov/pubmed/25157211
http://dx.doi.org/10.4137/JEN.S11269
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