Neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model

Abstract The pathophysiology of delayed carbon monoxide (CO) encephalopathy remains unclear. In this study, the effects of CO exposure on the dentate gyrus (DG) were investigated in a Wistar rat model by histochemical and molecular methods. Model rats showed significant cognitive impairment in the p...

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Autores principales:	Shinichiro Ochi, Keisuke Sekiya, Naoki Abe, Yu Funahashi, Hiroshi Kumon, Yuta Yoshino, Tasuku Nishihara, Shuken Boku, Jun-ichi Iga, Shu-ichi Ueno
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/573c594e6a9f463f8a84e134e0f948aa
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spelling	oai:doaj.org-article:573c594e6a9f463f8a84e134e0f948aa2021-12-02T11:39:44ZNeural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model10.1038/s41598-021-85860-92045-2322https://doaj.org/article/573c594e6a9f463f8a84e134e0f948aa2021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-85860-9https://doaj.org/toc/2045-2322Abstract The pathophysiology of delayed carbon monoxide (CO) encephalopathy remains unclear. In this study, the effects of CO exposure on the dentate gyrus (DG) were investigated in a Wistar rat model by histochemical and molecular methods. Model rats showed significant cognitive impairment in the passive-avoidance test beginning 7 days after CO exposure. Immunohistochemistry showed that compared to the control, the cell number of SRY (sex-determining region Y)-box 2 (SOX2)+/brain lipid binding protein (BLBP)+/glial fibrillary acidic protein (GFAP)+ cells in the DG was significantly less, but the number of SOX2+/GFAP− cells was not, reflecting a decreased number of type 1 and type 2a neural precursor cells. Compared to the control, the numbers of CD11b+ cells and neuron glial antigen 2+ cells were significantly less, but the number of SOX2−/GFAP+ cells was not. Flow cytometry showed that the percent of live microglial cells isolated from the hippocampus in this CO rat model was significantly lower than in controls. Furthermore, mRNA expression of fibroblast growth factor 2 and glial cell-derived neurotrophic factor, which are neurogenic factors, was significantly decreased in that area. We conclude that, in this rat model, there is an association between delayed cognitive impairment with dysregulated adult hippocampal neurogenesis and glial changes in delayed CO encephalopathy.Shinichiro OchiKeisuke SekiyaNaoki AbeYu FunahashiHiroshi KumonYuta YoshinoTasuku NishiharaShuken BokuJun-ichi IgaShu-ichi UenoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Shinichiro Ochi Keisuke Sekiya Naoki Abe Yu Funahashi Hiroshi Kumon Yuta Yoshino Tasuku Nishihara Shuken Boku Jun-ichi Iga Shu-ichi Ueno Neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model
description	Abstract The pathophysiology of delayed carbon monoxide (CO) encephalopathy remains unclear. In this study, the effects of CO exposure on the dentate gyrus (DG) were investigated in a Wistar rat model by histochemical and molecular methods. Model rats showed significant cognitive impairment in the passive-avoidance test beginning 7 days after CO exposure. Immunohistochemistry showed that compared to the control, the cell number of SRY (sex-determining region Y)-box 2 (SOX2)+/brain lipid binding protein (BLBP)+/glial fibrillary acidic protein (GFAP)+ cells in the DG was significantly less, but the number of SOX2+/GFAP− cells was not, reflecting a decreased number of type 1 and type 2a neural precursor cells. Compared to the control, the numbers of CD11b+ cells and neuron glial antigen 2+ cells were significantly less, but the number of SOX2−/GFAP+ cells was not. Flow cytometry showed that the percent of live microglial cells isolated from the hippocampus in this CO rat model was significantly lower than in controls. Furthermore, mRNA expression of fibroblast growth factor 2 and glial cell-derived neurotrophic factor, which are neurogenic factors, was significantly decreased in that area. We conclude that, in this rat model, there is an association between delayed cognitive impairment with dysregulated adult hippocampal neurogenesis and glial changes in delayed CO encephalopathy.
format	article
author	Shinichiro Ochi Keisuke Sekiya Naoki Abe Yu Funahashi Hiroshi Kumon Yuta Yoshino Tasuku Nishihara Shuken Boku Jun-ichi Iga Shu-ichi Ueno
author_facet	Shinichiro Ochi Keisuke Sekiya Naoki Abe Yu Funahashi Hiroshi Kumon Yuta Yoshino Tasuku Nishihara Shuken Boku Jun-ichi Iga Shu-ichi Ueno
author_sort	Shinichiro Ochi
title	Neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model
title_short	Neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model
title_full	Neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model
title_fullStr	Neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model
title_full_unstemmed	Neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model
title_sort	neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/573c594e6a9f463f8a84e134e0f948aa
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Neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model

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