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Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity

Various retinal injuries induced by ocular hypertension have been shown to induce plastic changes in retinal synapses, but the potential regulatory mechanism of synaptic plasticity after retinal injury was still unclear. A rat model of acute ocular hypertension was established by injecting saline in...

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Autores principales: Zhou, Lihong, Wang, Hui, Luo, Jia, Xiong, Kun, Zeng, Leping, Chen, Dan, Huang, Jufang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146193/
https://www.ncbi.nlm.nih.gov/pubmed/25206825
http://dx.doi.org/10.4103/1673-5374.128240
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author Zhou, Lihong
Wang, Hui
Luo, Jia
Xiong, Kun
Zeng, Leping
Chen, Dan
Huang, Jufang
author_facet Zhou, Lihong
Wang, Hui
Luo, Jia
Xiong, Kun
Zeng, Leping
Chen, Dan
Huang, Jufang
author_sort Zhou, Lihong
collection PubMed
description Various retinal injuries induced by ocular hypertension have been shown to induce plastic changes in retinal synapses, but the potential regulatory mechanism of synaptic plasticity after retinal injury was still unclear. A rat model of acute ocular hypertension was established by injecting saline intravitreally for an hour, and elevating the intraocular pressure to 14.63 kPa (110 mmHg). Western blot assay and immunofluorescence results showed that synaptophysin expression had a distinct spatiotemporal change that increased in the inner plexiform layer within 1 day and spread across the outer plexiform layer after 3 days. Glial fibrillary acidic protein expression in retinae was greatly increased after 3 days, and reached a peak at 7 days, which was also consistent with the peak time of synaptophysin expression in the outer plexiform layer following the increased intraocular pressure. Fluorocitrate, a glial metabolic inhibitor, was intravitreally injected to inhibit glial cell activation following high intraocular pressure. This significantly inhibited the enhanced glial fibrillary acidic protein expression induced by high intraocular pressure injury. Synaptophysin expression also decreased in the inner plexiform layer within a day and the widened distribution in the outer plexiform layer had disappeared by 3 days. The results suggested that retinal glial cell activation might play an important role in the process of retinal synaptic plasticity induced by acute high intraocular pressure through affecting the expression and distribution of synaptic functional proteins, such as synaptophysin.
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spelling pubmed-41461932014-09-09 Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity Zhou, Lihong Wang, Hui Luo, Jia Xiong, Kun Zeng, Leping Chen, Dan Huang, Jufang Neural Regen Res Research and Report Various retinal injuries induced by ocular hypertension have been shown to induce plastic changes in retinal synapses, but the potential regulatory mechanism of synaptic plasticity after retinal injury was still unclear. A rat model of acute ocular hypertension was established by injecting saline intravitreally for an hour, and elevating the intraocular pressure to 14.63 kPa (110 mmHg). Western blot assay and immunofluorescence results showed that synaptophysin expression had a distinct spatiotemporal change that increased in the inner plexiform layer within 1 day and spread across the outer plexiform layer after 3 days. Glial fibrillary acidic protein expression in retinae was greatly increased after 3 days, and reached a peak at 7 days, which was also consistent with the peak time of synaptophysin expression in the outer plexiform layer following the increased intraocular pressure. Fluorocitrate, a glial metabolic inhibitor, was intravitreally injected to inhibit glial cell activation following high intraocular pressure. This significantly inhibited the enhanced glial fibrillary acidic protein expression induced by high intraocular pressure injury. Synaptophysin expression also decreased in the inner plexiform layer within a day and the widened distribution in the outer plexiform layer had disappeared by 3 days. The results suggested that retinal glial cell activation might play an important role in the process of retinal synaptic plasticity induced by acute high intraocular pressure through affecting the expression and distribution of synaptic functional proteins, such as synaptophysin. Medknow Publications & Media Pvt Ltd 2014-02-15 /pmc/articles/PMC4146193/ /pubmed/25206825 http://dx.doi.org/10.4103/1673-5374.128240 Text en Copyright: © Neural Regeneration Research http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research and Report
Zhou, Lihong
Wang, Hui
Luo, Jia
Xiong, Kun
Zeng, Leping
Chen, Dan
Huang, Jufang
Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity
title Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity
title_full Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity
title_fullStr Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity
title_full_unstemmed Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity
title_short Regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity
title_sort regulatory effects of inhibiting the activation of glial cells on retinal synaptic plasticity
topic Research and Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146193/
https://www.ncbi.nlm.nih.gov/pubmed/25206825
http://dx.doi.org/10.4103/1673-5374.128240
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