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Classification of Visual Cortex Plasticity Phenotypes following Treatment for Amblyopia
Monocular deprivation (MD) during the critical period (CP) has enduring effects on visual acuity and the functioning of the visual cortex (V1). This experience-dependent plasticity has become a model for studying the mechanisms, especially glutamatergic and GABAergic receptors, that regulate amblyop...
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/PMC6746165/ https://www.ncbi.nlm.nih.gov/pubmed/31565045 http://dx.doi.org/10.1155/2019/2564018 |
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author | Balsor, Justin L. Jones, David G. Murphy, Kathryn M. |
author_facet | Balsor, Justin L. Jones, David G. Murphy, Kathryn M. |
author_sort | Balsor, Justin L. |
collection | PubMed |
description | Monocular deprivation (MD) during the critical period (CP) has enduring effects on visual acuity and the functioning of the visual cortex (V1). This experience-dependent plasticity has become a model for studying the mechanisms, especially glutamatergic and GABAergic receptors, that regulate amblyopia. Less is known, however, about treatment-induced changes to those receptors and if those changes differentiate treatments that support the recovery of acuity versus persistent acuity deficits. Here, we use an animal model to explore the effects of 3 visual treatments started during the CP (n = 24, 10 male and 14 female): binocular vision (BV) that promotes good acuity versus reverse occlusion (RO) and binocular deprivation (BD) that causes persistent acuity deficits. We measured the recovery of a collection of glutamatergic and GABAergic receptor subunits in the V1 and modeled recovery of kinetics for NMDAR and GABA(A)R. There was a complex pattern of protein changes that prompted us to develop an unbiased data-driven approach for these high-dimensional data analyses to identify plasticity features and construct plasticity phenotypes. Cluster analysis of the plasticity phenotypes suggests that BV supports adaptive plasticity while RO and BD promote a maladaptive pattern. The RO plasticity phenotype appeared more similar to adults with a high expression of GluA2, and the BD phenotypes were dominated by GABA(A)α1, highlighting that multiple plasticity phenotypes can underlie persistent poor acuity. After 2-4 days of BV, the plasticity phenotypes resembled normals, but only one feature, the GluN2A:GluA2 balance, returned to normal levels. Perhaps, balancing Hebbian (GluN2A) and homeostatic (GluA2) mechanisms is necessary for the recovery of vision. |
format | Online Article Text |
id | pubmed-6746165 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-67461652019-09-29 Classification of Visual Cortex Plasticity Phenotypes following Treatment for Amblyopia Balsor, Justin L. Jones, David G. Murphy, Kathryn M. Neural Plast Research Article Monocular deprivation (MD) during the critical period (CP) has enduring effects on visual acuity and the functioning of the visual cortex (V1). This experience-dependent plasticity has become a model for studying the mechanisms, especially glutamatergic and GABAergic receptors, that regulate amblyopia. Less is known, however, about treatment-induced changes to those receptors and if those changes differentiate treatments that support the recovery of acuity versus persistent acuity deficits. Here, we use an animal model to explore the effects of 3 visual treatments started during the CP (n = 24, 10 male and 14 female): binocular vision (BV) that promotes good acuity versus reverse occlusion (RO) and binocular deprivation (BD) that causes persistent acuity deficits. We measured the recovery of a collection of glutamatergic and GABAergic receptor subunits in the V1 and modeled recovery of kinetics for NMDAR and GABA(A)R. There was a complex pattern of protein changes that prompted us to develop an unbiased data-driven approach for these high-dimensional data analyses to identify plasticity features and construct plasticity phenotypes. Cluster analysis of the plasticity phenotypes suggests that BV supports adaptive plasticity while RO and BD promote a maladaptive pattern. The RO plasticity phenotype appeared more similar to adults with a high expression of GluA2, and the BD phenotypes were dominated by GABA(A)α1, highlighting that multiple plasticity phenotypes can underlie persistent poor acuity. After 2-4 days of BV, the plasticity phenotypes resembled normals, but only one feature, the GluN2A:GluA2 balance, returned to normal levels. Perhaps, balancing Hebbian (GluN2A) and homeostatic (GluA2) mechanisms is necessary for the recovery of vision. Hindawi 2019-09-03 /pmc/articles/PMC6746165/ /pubmed/31565045 http://dx.doi.org/10.1155/2019/2564018 Text en Copyright © 2019 Justin L. Balsor 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 Balsor, Justin L. Jones, David G. Murphy, Kathryn M. Classification of Visual Cortex Plasticity Phenotypes following Treatment for Amblyopia |
title | Classification of Visual Cortex Plasticity Phenotypes following Treatment for Amblyopia |
title_full | Classification of Visual Cortex Plasticity Phenotypes following Treatment for Amblyopia |
title_fullStr | Classification of Visual Cortex Plasticity Phenotypes following Treatment for Amblyopia |
title_full_unstemmed | Classification of Visual Cortex Plasticity Phenotypes following Treatment for Amblyopia |
title_short | Classification of Visual Cortex Plasticity Phenotypes following Treatment for Amblyopia |
title_sort | classification of visual cortex plasticity phenotypes following treatment for amblyopia |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6746165/ https://www.ncbi.nlm.nih.gov/pubmed/31565045 http://dx.doi.org/10.1155/2019/2564018 |
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