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The increased expression of GABA receptors within the arcuate nucleus is associated with high intraocular pressure

PURPOSE: To investigate the relationship between intraocular pressure (IOP) and GABA receptors within the arcuate nucleus (ARC). METHODS: In the chronic high IOP rat model, ibotenic acid (IBO) was injected to induce impairment of the ARC, and IOP was measured at the 0, 1, 2, 3, and 4 week time point...

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Autores principales: Gong, Jie-Ling, Lou, Xiao-Tong, Yuan, Yu-Xiang, Chen, Li-Wen, Ji, Ping-Ting, Li, Lu, Zhao, Yin, Zhang, Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Vision 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6107798/
https://www.ncbi.nlm.nih.gov/pubmed/30174387
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author Gong, Jie-Ling
Lou, Xiao-Tong
Yuan, Yu-Xiang
Chen, Li-Wen
Ji, Ping-Ting
Li, Lu
Zhao, Yin
Zhang, Hong
author_facet Gong, Jie-Ling
Lou, Xiao-Tong
Yuan, Yu-Xiang
Chen, Li-Wen
Ji, Ping-Ting
Li, Lu
Zhao, Yin
Zhang, Hong
author_sort Gong, Jie-Ling
collection PubMed
description PURPOSE: To investigate the relationship between intraocular pressure (IOP) and GABA receptors within the arcuate nucleus (ARC). METHODS: In the chronic high IOP rat model, ibotenic acid (IBO) was injected to induce impairment of the ARC, and IOP was measured at the 0, 1, 2, 3, and 4 week time points with a Tono-Pen. To assess the expression of GABA-A/B receptors within the ARC under persistent high IOP, we performed immunofluorescence (IF) and immunohistochemical (IHC) staining at 2 weeks and 4 weeks. Furthermore, we treated the ARC with GABA-A/B receptor antagonists separately, and IOP was evaluated, as well as retinal ganglion cell apoptosis in the chronic high IOP rat model. In the following induced high IOP animal model, the expression of GABA-A/B receptors within the ARC was evaluated in DBA/2J mice which developed progressive eye abnormalities spontaneously that closely mimic human hereditary glaucoma. RESULTS: Compared with the control group, statistically significant downregulation of IOP was noted due to the IBO injection into the ARC at the 2, 3, and 4 week time points (p<0.05). Persistent high IOP elicited increased expression of the GABA-A/B receptors in the ARC compared with the control group (p<0.01). In addition, treatment with GABA-A/B receptor antagonists separately caused a decrease in the IOP, along with reduced retinal ganglion cell apoptosis (p<0.01). In the DBA/2J mice, the expression of the GABA receptors was statistically significantly increased (p<0.01). CONCLUSIONS: GABA-A/B receptors in the ARC may be involved in regulation of IOP, and pathologically high IOP affects the expression of GABA-A/B receptors in the ARC.
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spelling pubmed-61077982018-08-31 The increased expression of GABA receptors within the arcuate nucleus is associated with high intraocular pressure Gong, Jie-Ling Lou, Xiao-Tong Yuan, Yu-Xiang Chen, Li-Wen Ji, Ping-Ting Li, Lu Zhao, Yin Zhang, Hong Mol Vis Research Article PURPOSE: To investigate the relationship between intraocular pressure (IOP) and GABA receptors within the arcuate nucleus (ARC). METHODS: In the chronic high IOP rat model, ibotenic acid (IBO) was injected to induce impairment of the ARC, and IOP was measured at the 0, 1, 2, 3, and 4 week time points with a Tono-Pen. To assess the expression of GABA-A/B receptors within the ARC under persistent high IOP, we performed immunofluorescence (IF) and immunohistochemical (IHC) staining at 2 weeks and 4 weeks. Furthermore, we treated the ARC with GABA-A/B receptor antagonists separately, and IOP was evaluated, as well as retinal ganglion cell apoptosis in the chronic high IOP rat model. In the following induced high IOP animal model, the expression of GABA-A/B receptors within the ARC was evaluated in DBA/2J mice which developed progressive eye abnormalities spontaneously that closely mimic human hereditary glaucoma. RESULTS: Compared with the control group, statistically significant downregulation of IOP was noted due to the IBO injection into the ARC at the 2, 3, and 4 week time points (p<0.05). Persistent high IOP elicited increased expression of the GABA-A/B receptors in the ARC compared with the control group (p<0.01). In addition, treatment with GABA-A/B receptor antagonists separately caused a decrease in the IOP, along with reduced retinal ganglion cell apoptosis (p<0.01). In the DBA/2J mice, the expression of the GABA receptors was statistically significantly increased (p<0.01). CONCLUSIONS: GABA-A/B receptors in the ARC may be involved in regulation of IOP, and pathologically high IOP affects the expression of GABA-A/B receptors in the ARC. Molecular Vision 2018-08-15 /pmc/articles/PMC6107798/ /pubmed/30174387 Text en Copyright © 2018 Molecular Vision. http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited, used for non-commercial purposes, and is not altered or transformed.
spellingShingle Research Article
Gong, Jie-Ling
Lou, Xiao-Tong
Yuan, Yu-Xiang
Chen, Li-Wen
Ji, Ping-Ting
Li, Lu
Zhao, Yin
Zhang, Hong
The increased expression of GABA receptors within the arcuate nucleus is associated with high intraocular pressure
title The increased expression of GABA receptors within the arcuate nucleus is associated with high intraocular pressure
title_full The increased expression of GABA receptors within the arcuate nucleus is associated with high intraocular pressure
title_fullStr The increased expression of GABA receptors within the arcuate nucleus is associated with high intraocular pressure
title_full_unstemmed The increased expression of GABA receptors within the arcuate nucleus is associated with high intraocular pressure
title_short The increased expression of GABA receptors within the arcuate nucleus is associated with high intraocular pressure
title_sort increased expression of gaba receptors within the arcuate nucleus is associated with high intraocular pressure
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6107798/
https://www.ncbi.nlm.nih.gov/pubmed/30174387
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