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Excess Glutamate May Cause Dilation of Retinal Blood Vessels in Glutamate/Aspartate Transporter-Deficient Mice
PURPOSE: To investigate the longitudinal findings of fundus features and spectral-domain optical coherence tomography (SD-OCT) to characterize the morphologic features in a mouse model of defective glutamate/aspartate transporter (GLAST(−/−) mice). MATERIALS AND METHODS: The fundus findings and SD-O...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6881573/ https://www.ncbi.nlm.nih.gov/pubmed/31828115 http://dx.doi.org/10.1155/2019/6512195 |
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author | Gonome, Takayuki Xie, Yuting Arai, Saeko Yamauchi, Kodai Maeda-Monai, Natsuki Tanabu, Reiko Kudo, Takashi Nakazawa, Mitsuru |
author_facet | Gonome, Takayuki Xie, Yuting Arai, Saeko Yamauchi, Kodai Maeda-Monai, Natsuki Tanabu, Reiko Kudo, Takashi Nakazawa, Mitsuru |
author_sort | Gonome, Takayuki |
collection | PubMed |
description | PURPOSE: To investigate the longitudinal findings of fundus features and spectral-domain optical coherence tomography (SD-OCT) to characterize the morphologic features in a mouse model of defective glutamate/aspartate transporter (GLAST(−/−) mice). MATERIALS AND METHODS: The fundus findings and SD-OCT images were longitudinally recorded at five time points from postnatal (P) 22 to P156 in GLAST(−/−) mice. As a control wild type, age-matched C57BL/6J mice were employed. The mouse retina was subdivided into five layers, and the thickness of each layer was longitudinally measured by InSight® using SD-OCT pictures. The SD-OCT findings were compared with the histologic appearances. The diameter of the retinal blood vessels was measured by the ImageJ® software program using SD-OCT images. The data were statistically compared between both age-matched mouse groups. RESULTS: The retinal blood vessels appeared more dilated in GLAST(−/−) mice than in wild-type mice. This tendency was statistically significant at all time points after P44 by analyses using SD-OCT images. The ganglion cell complex (GCC) and outer nuclear layer (ONL) were significantly thinner in GLAST(−/−) mice at all time points after P80 than in the wild-type mice. This tendency was more clearly indicated by SD-OCT than histologic sections. DISCUSSION: In the present study, we found for the first time the dilation of the retinal blood vessels and the thinning of the ONL in GLAST(−/−) mice, in addition to the thinning of the GCC. |
format | Online Article Text |
id | pubmed-6881573 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-68815732019-12-11 Excess Glutamate May Cause Dilation of Retinal Blood Vessels in Glutamate/Aspartate Transporter-Deficient Mice Gonome, Takayuki Xie, Yuting Arai, Saeko Yamauchi, Kodai Maeda-Monai, Natsuki Tanabu, Reiko Kudo, Takashi Nakazawa, Mitsuru Biomed Res Int Research Article PURPOSE: To investigate the longitudinal findings of fundus features and spectral-domain optical coherence tomography (SD-OCT) to characterize the morphologic features in a mouse model of defective glutamate/aspartate transporter (GLAST(−/−) mice). MATERIALS AND METHODS: The fundus findings and SD-OCT images were longitudinally recorded at five time points from postnatal (P) 22 to P156 in GLAST(−/−) mice. As a control wild type, age-matched C57BL/6J mice were employed. The mouse retina was subdivided into five layers, and the thickness of each layer was longitudinally measured by InSight® using SD-OCT pictures. The SD-OCT findings were compared with the histologic appearances. The diameter of the retinal blood vessels was measured by the ImageJ® software program using SD-OCT images. The data were statistically compared between both age-matched mouse groups. RESULTS: The retinal blood vessels appeared more dilated in GLAST(−/−) mice than in wild-type mice. This tendency was statistically significant at all time points after P44 by analyses using SD-OCT images. The ganglion cell complex (GCC) and outer nuclear layer (ONL) were significantly thinner in GLAST(−/−) mice at all time points after P80 than in the wild-type mice. This tendency was more clearly indicated by SD-OCT than histologic sections. DISCUSSION: In the present study, we found for the first time the dilation of the retinal blood vessels and the thinning of the ONL in GLAST(−/−) mice, in addition to the thinning of the GCC. Hindawi 2019-11-11 /pmc/articles/PMC6881573/ /pubmed/31828115 http://dx.doi.org/10.1155/2019/6512195 Text en Copyright © 2019 Takayuki Gonome et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Gonome, Takayuki Xie, Yuting Arai, Saeko Yamauchi, Kodai Maeda-Monai, Natsuki Tanabu, Reiko Kudo, Takashi Nakazawa, Mitsuru Excess Glutamate May Cause Dilation of Retinal Blood Vessels in Glutamate/Aspartate Transporter-Deficient Mice |
title | Excess Glutamate May Cause Dilation of Retinal Blood Vessels in Glutamate/Aspartate Transporter-Deficient Mice |
title_full | Excess Glutamate May Cause Dilation of Retinal Blood Vessels in Glutamate/Aspartate Transporter-Deficient Mice |
title_fullStr | Excess Glutamate May Cause Dilation of Retinal Blood Vessels in Glutamate/Aspartate Transporter-Deficient Mice |
title_full_unstemmed | Excess Glutamate May Cause Dilation of Retinal Blood Vessels in Glutamate/Aspartate Transporter-Deficient Mice |
title_short | Excess Glutamate May Cause Dilation of Retinal Blood Vessels in Glutamate/Aspartate Transporter-Deficient Mice |
title_sort | excess glutamate may cause dilation of retinal blood vessels in glutamate/aspartate transporter-deficient mice |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6881573/ https://www.ncbi.nlm.nih.gov/pubmed/31828115 http://dx.doi.org/10.1155/2019/6512195 |
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