EAAC1 gene deletion reduces adult hippocampal neurogenesis after transient cerebral ischemia

Abstract Several studies have demonstrated that excitatory amino acid carrier-1 (EAAC1) gene deletion exacerbates hippocampal and cortical neuronal death after ischemia. However, presently there are no studies investigating the role of EAAC1 in hippocampal neurogenesis. In this study, we tested the...

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Autores principales:	Bo Young Choi, Seok Joon Won, Jin Hee Kim, Min Sohn, Hong Ki Song, Tae Nyoung Chung, Tae Yul Kim, Sang Won Suh
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/6186973f51dc4d5b987b9a1260c82479
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spelling	oai:doaj.org-article:6186973f51dc4d5b987b9a1260c824792021-12-02T16:08:03ZEAAC1 gene deletion reduces adult hippocampal neurogenesis after transient cerebral ischemia10.1038/s41598-018-25191-42045-2322https://doaj.org/article/6186973f51dc4d5b987b9a1260c824792018-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-25191-4https://doaj.org/toc/2045-2322Abstract Several studies have demonstrated that excitatory amino acid carrier-1 (EAAC1) gene deletion exacerbates hippocampal and cortical neuronal death after ischemia. However, presently there are no studies investigating the role of EAAC1 in hippocampal neurogenesis. In this study, we tested the hypothesis that reduced cysteine transport into neurons by EAAC1 knockout negatively affects adult hippocampal neurogenesis under physiological or pathological states. This study used young mice (aged 3–5 months) and aged mice (aged 11–15 months) of either the wild-type (WT) or EAAC1 −/− genotype. Ischemia was induced through the occlusion of bilateral common carotid arteries for 30 minutes. Histological analysis was performed at 7 or 30 days after ischemia. We found that both young and aged mice with loss of the EAAC1 displayed unaltered cell proliferation and neuronal differentiation, as compared to age-matched WT mice under ischemia-free conditions. However, neurons generated from EAAC1 −/− mice showed poor survival outcomes in both young and aged mice. In addition, deletion of EAAC1 reduced the overall level of neurogenesis, including cell proliferation, differentiation, and survival after ischemia. The present study demonstrates that EAAC1 is important for the survival of newly generated neurons in the adult brain under physiological and pathological conditions. Therefore, this study suggests that EAAC1 plays an essential role in modulating hippocampal neurogenesis.Bo Young ChoiSeok Joon WonJin Hee KimMin SohnHong Ki SongTae Nyoung ChungTae Yul KimSang Won SuhNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-12 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Bo Young Choi Seok Joon Won Jin Hee Kim Min Sohn Hong Ki Song Tae Nyoung Chung Tae Yul Kim Sang Won Suh EAAC1 gene deletion reduces adult hippocampal neurogenesis after transient cerebral ischemia
description	Abstract Several studies have demonstrated that excitatory amino acid carrier-1 (EAAC1) gene deletion exacerbates hippocampal and cortical neuronal death after ischemia. However, presently there are no studies investigating the role of EAAC1 in hippocampal neurogenesis. In this study, we tested the hypothesis that reduced cysteine transport into neurons by EAAC1 knockout negatively affects adult hippocampal neurogenesis under physiological or pathological states. This study used young mice (aged 3–5 months) and aged mice (aged 11–15 months) of either the wild-type (WT) or EAAC1 −/− genotype. Ischemia was induced through the occlusion of bilateral common carotid arteries for 30 minutes. Histological analysis was performed at 7 or 30 days after ischemia. We found that both young and aged mice with loss of the EAAC1 displayed unaltered cell proliferation and neuronal differentiation, as compared to age-matched WT mice under ischemia-free conditions. However, neurons generated from EAAC1 −/− mice showed poor survival outcomes in both young and aged mice. In addition, deletion of EAAC1 reduced the overall level of neurogenesis, including cell proliferation, differentiation, and survival after ischemia. The present study demonstrates that EAAC1 is important for the survival of newly generated neurons in the adult brain under physiological and pathological conditions. Therefore, this study suggests that EAAC1 plays an essential role in modulating hippocampal neurogenesis.
format	article
author	Bo Young Choi Seok Joon Won Jin Hee Kim Min Sohn Hong Ki Song Tae Nyoung Chung Tae Yul Kim Sang Won Suh
author_facet	Bo Young Choi Seok Joon Won Jin Hee Kim Min Sohn Hong Ki Song Tae Nyoung Chung Tae Yul Kim Sang Won Suh
author_sort	Bo Young Choi
title	EAAC1 gene deletion reduces adult hippocampal neurogenesis after transient cerebral ischemia
title_short	EAAC1 gene deletion reduces adult hippocampal neurogenesis after transient cerebral ischemia
title_full	EAAC1 gene deletion reduces adult hippocampal neurogenesis after transient cerebral ischemia
title_fullStr	EAAC1 gene deletion reduces adult hippocampal neurogenesis after transient cerebral ischemia
title_full_unstemmed	EAAC1 gene deletion reduces adult hippocampal neurogenesis after transient cerebral ischemia
title_sort	eaac1 gene deletion reduces adult hippocampal neurogenesis after transient cerebral ischemia
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/6186973f51dc4d5b987b9a1260c82479
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EAAC1 gene deletion reduces adult hippocampal neurogenesis after transient cerebral ischemia

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