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Enriched Environment Promoted Cognitive Function via Bilateral Synaptic Remodeling After Cerebral Ischemia

Ischemic stroke is the second leading cause of death worldwide. Ischemia-induced cognitive dysfunction may result in a poor quality of life. Synaptic plasticity plays a key role in cognition promotion. An enriched environment (EE), which can attenuate cognitive deficits in chronic cerebral hypoperfu...

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Autores principales: Wang, Chuanjie, Zhang, Qun, Yu, Kewei, Shen, Xueyan, Wu, Yi, Wu, Junfa
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6861441/
https://www.ncbi.nlm.nih.gov/pubmed/31781025
http://dx.doi.org/10.3389/fneur.2019.01189
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author Wang, Chuanjie
Zhang, Qun
Yu, Kewei
Shen, Xueyan
Wu, Yi
Wu, Junfa
author_facet Wang, Chuanjie
Zhang, Qun
Yu, Kewei
Shen, Xueyan
Wu, Yi
Wu, Junfa
author_sort Wang, Chuanjie
collection PubMed
description Ischemic stroke is the second leading cause of death worldwide. Ischemia-induced cognitive dysfunction may result in a poor quality of life. Synaptic plasticity plays a key role in cognition promotion. An enriched environment (EE), which can attenuate cognitive deficits in chronic cerebral hypoperfusion, has been shown to facilitate synaptic plasticity. However, the effect of EE on synaptic plasticity in bilateral cerebral hemispheres in stroke remains unclear. This study used a permanent middle cerebral artery occlusion mouse model, which was divided into standard housing and EE groups. The Morris water maze test was performed to detect the cognitive function. Electron microscopy was used to determine the synapse numbers. The expression of SYN and GAP-43 was then quantified by immunofluorescence staining and Western blot analysis. Compared with the standard housing, EE promoted the cognitive function recovery in the mice with stroke. Moreover, EE increased the synapse numbers and the expression of SYN and GAP-43 in both the ipsilateral and contralateral hemispheres (P < 0.05). A further correlation analysis revealed a positive correlation between the cognitive function outcomes and the relative expression of GAP-43 and SYN. Furthermore, the correlation of the expression of GAP-43 and SYN with cognitive function was higher in the contralateral brain than in the ipsilateral brain. In conclusion, an EE may promote cognitive function via bilateral synaptic remodeling after cerebral ischemia. Also, the contralateral brain may play an important role in the recovery of cognitive function.
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spelling pubmed-68614412019-11-28 Enriched Environment Promoted Cognitive Function via Bilateral Synaptic Remodeling After Cerebral Ischemia Wang, Chuanjie Zhang, Qun Yu, Kewei Shen, Xueyan Wu, Yi Wu, Junfa Front Neurol Neurology Ischemic stroke is the second leading cause of death worldwide. Ischemia-induced cognitive dysfunction may result in a poor quality of life. Synaptic plasticity plays a key role in cognition promotion. An enriched environment (EE), which can attenuate cognitive deficits in chronic cerebral hypoperfusion, has been shown to facilitate synaptic plasticity. However, the effect of EE on synaptic plasticity in bilateral cerebral hemispheres in stroke remains unclear. This study used a permanent middle cerebral artery occlusion mouse model, which was divided into standard housing and EE groups. The Morris water maze test was performed to detect the cognitive function. Electron microscopy was used to determine the synapse numbers. The expression of SYN and GAP-43 was then quantified by immunofluorescence staining and Western blot analysis. Compared with the standard housing, EE promoted the cognitive function recovery in the mice with stroke. Moreover, EE increased the synapse numbers and the expression of SYN and GAP-43 in both the ipsilateral and contralateral hemispheres (P < 0.05). A further correlation analysis revealed a positive correlation between the cognitive function outcomes and the relative expression of GAP-43 and SYN. Furthermore, the correlation of the expression of GAP-43 and SYN with cognitive function was higher in the contralateral brain than in the ipsilateral brain. In conclusion, an EE may promote cognitive function via bilateral synaptic remodeling after cerebral ischemia. Also, the contralateral brain may play an important role in the recovery of cognitive function. Frontiers Media S.A. 2019-11-12 /pmc/articles/PMC6861441/ /pubmed/31781025 http://dx.doi.org/10.3389/fneur.2019.01189 Text en Copyright © 2019 Wang, Zhang, Yu, Shen, Wu and Wu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neurology
Wang, Chuanjie
Zhang, Qun
Yu, Kewei
Shen, Xueyan
Wu, Yi
Wu, Junfa
Enriched Environment Promoted Cognitive Function via Bilateral Synaptic Remodeling After Cerebral Ischemia
title Enriched Environment Promoted Cognitive Function via Bilateral Synaptic Remodeling After Cerebral Ischemia
title_full Enriched Environment Promoted Cognitive Function via Bilateral Synaptic Remodeling After Cerebral Ischemia
title_fullStr Enriched Environment Promoted Cognitive Function via Bilateral Synaptic Remodeling After Cerebral Ischemia
title_full_unstemmed Enriched Environment Promoted Cognitive Function via Bilateral Synaptic Remodeling After Cerebral Ischemia
title_short Enriched Environment Promoted Cognitive Function via Bilateral Synaptic Remodeling After Cerebral Ischemia
title_sort enriched environment promoted cognitive function via bilateral synaptic remodeling after cerebral ischemia
topic Neurology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6861441/
https://www.ncbi.nlm.nih.gov/pubmed/31781025
http://dx.doi.org/10.3389/fneur.2019.01189
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