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Spatiotemporal profile of Map2 and microglial changes in the hippocampal CA1 region following pilocarpine-induced status epilepticus

Status epilepticus (SE) triggers pathological changes to hippocampal dendrites that may promote epileptogenesis. The microtubule associated protein 2 (Map2) helps stabilize microtubules of the dendritic cytoskeleton. Recently, we reported a substantial decline in Map2 that coincided with robust micr...

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Autores principales: Schartz, Nicole D., Herr, Seth A., Madsen, Lauren, Butts, Sarah J., Torres, Ceidy, Mendez, Loyda B., Brewster, Amy L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855223/
https://www.ncbi.nlm.nih.gov/pubmed/27143585
http://dx.doi.org/10.1038/srep24988
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author Schartz, Nicole D.
Herr, Seth A.
Madsen, Lauren
Butts, Sarah J.
Torres, Ceidy
Mendez, Loyda B.
Brewster, Amy L.
author_facet Schartz, Nicole D.
Herr, Seth A.
Madsen, Lauren
Butts, Sarah J.
Torres, Ceidy
Mendez, Loyda B.
Brewster, Amy L.
author_sort Schartz, Nicole D.
collection PubMed
description Status epilepticus (SE) triggers pathological changes to hippocampal dendrites that may promote epileptogenesis. The microtubule associated protein 2 (Map2) helps stabilize microtubules of the dendritic cytoskeleton. Recently, we reported a substantial decline in Map2 that coincided with robust microglia accumulation in the CA1 hippocampal region after an episode of SE. A spatial correlation between Map2 loss and reactive microglia was also reported in human cortex from refractory epilepsy. New evidence supports that microglia modulate dendritic structures. Thus, to identify a potential association between SE-induced Map2 and microglial changes, a spatiotemporal profile of these events is necessary. We used immunohistochemistry to determine the distribution of Map2 and the microglia marker IBA1 in the hippocampus after pilocarpine-induced SE from 4 hrs to 35 days. We found a decline in Map2 immunoreactivity in the CA1 area that reached minimal levels at 14 days post-SE and partially increased thereafter. In contrast, maximal microglia accumulation occurred in the CA1 area at 14 days post-SE. Our data indicate that SE-induced Map2 and microglial changes parallel each other’s spatiotemporal profiles. These findings may lay the foundation for future mechanistic studies to help identify potential roles for microglia in the dendritic pathology associated with SE and epilepsy.
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spelling pubmed-48552232016-05-18 Spatiotemporal profile of Map2 and microglial changes in the hippocampal CA1 region following pilocarpine-induced status epilepticus Schartz, Nicole D. Herr, Seth A. Madsen, Lauren Butts, Sarah J. Torres, Ceidy Mendez, Loyda B. Brewster, Amy L. Sci Rep Article Status epilepticus (SE) triggers pathological changes to hippocampal dendrites that may promote epileptogenesis. The microtubule associated protein 2 (Map2) helps stabilize microtubules of the dendritic cytoskeleton. Recently, we reported a substantial decline in Map2 that coincided with robust microglia accumulation in the CA1 hippocampal region after an episode of SE. A spatial correlation between Map2 loss and reactive microglia was also reported in human cortex from refractory epilepsy. New evidence supports that microglia modulate dendritic structures. Thus, to identify a potential association between SE-induced Map2 and microglial changes, a spatiotemporal profile of these events is necessary. We used immunohistochemistry to determine the distribution of Map2 and the microglia marker IBA1 in the hippocampus after pilocarpine-induced SE from 4 hrs to 35 days. We found a decline in Map2 immunoreactivity in the CA1 area that reached minimal levels at 14 days post-SE and partially increased thereafter. In contrast, maximal microglia accumulation occurred in the CA1 area at 14 days post-SE. Our data indicate that SE-induced Map2 and microglial changes parallel each other’s spatiotemporal profiles. These findings may lay the foundation for future mechanistic studies to help identify potential roles for microglia in the dendritic pathology associated with SE and epilepsy. Nature Publishing Group 2016-05-04 /pmc/articles/PMC4855223/ /pubmed/27143585 http://dx.doi.org/10.1038/srep24988 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Schartz, Nicole D.
Herr, Seth A.
Madsen, Lauren
Butts, Sarah J.
Torres, Ceidy
Mendez, Loyda B.
Brewster, Amy L.
Spatiotemporal profile of Map2 and microglial changes in the hippocampal CA1 region following pilocarpine-induced status epilepticus
title Spatiotemporal profile of Map2 and microglial changes in the hippocampal CA1 region following pilocarpine-induced status epilepticus
title_full Spatiotemporal profile of Map2 and microglial changes in the hippocampal CA1 region following pilocarpine-induced status epilepticus
title_fullStr Spatiotemporal profile of Map2 and microglial changes in the hippocampal CA1 region following pilocarpine-induced status epilepticus
title_full_unstemmed Spatiotemporal profile of Map2 and microglial changes in the hippocampal CA1 region following pilocarpine-induced status epilepticus
title_short Spatiotemporal profile of Map2 and microglial changes in the hippocampal CA1 region following pilocarpine-induced status epilepticus
title_sort spatiotemporal profile of map2 and microglial changes in the hippocampal ca1 region following pilocarpine-induced status epilepticus
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855223/
https://www.ncbi.nlm.nih.gov/pubmed/27143585
http://dx.doi.org/10.1038/srep24988
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