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Synaptic remodeling of neuronal circuits in early retinal degeneration

Photoreceptor degenerations are a major cause of blindness and among the most common forms of neurodegeneration in humans. Studies of mouse models revealed that synaptic dysfunction often precedes photoreceptor degeneration, and that abnormal synaptic input from photoreceptors to bipolar cells cause...

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Detalles Bibliográficos
Autores principales: Soto, Florentina, Kerschensteiner, Daniel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4595653/
https://www.ncbi.nlm.nih.gov/pubmed/26500497
http://dx.doi.org/10.3389/fncel.2015.00395
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author Soto, Florentina
Kerschensteiner, Daniel
author_facet Soto, Florentina
Kerschensteiner, Daniel
author_sort Soto, Florentina
collection PubMed
description Photoreceptor degenerations are a major cause of blindness and among the most common forms of neurodegeneration in humans. Studies of mouse models revealed that synaptic dysfunction often precedes photoreceptor degeneration, and that abnormal synaptic input from photoreceptors to bipolar cells causes circuits in the inner retina to become hyperactive. Here, we provide a brief overview of frequently used mouse models of photoreceptor degenerations. We then discuss insights into circuit remodeling triggered by early synaptic dysfunction in the outer and hyperactivity in the inner retina. We discuss these insights in the context of other experimental manipulations of synaptic function and activity. Knowledge of the plasticity and early remodeling of retinal circuits will be critical for the design of successful vision rescue strategies.
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spelling pubmed-45956532015-10-23 Synaptic remodeling of neuronal circuits in early retinal degeneration Soto, Florentina Kerschensteiner, Daniel Front Cell Neurosci Neuroscience Photoreceptor degenerations are a major cause of blindness and among the most common forms of neurodegeneration in humans. Studies of mouse models revealed that synaptic dysfunction often precedes photoreceptor degeneration, and that abnormal synaptic input from photoreceptors to bipolar cells causes circuits in the inner retina to become hyperactive. Here, we provide a brief overview of frequently used mouse models of photoreceptor degenerations. We then discuss insights into circuit remodeling triggered by early synaptic dysfunction in the outer and hyperactivity in the inner retina. We discuss these insights in the context of other experimental manipulations of synaptic function and activity. Knowledge of the plasticity and early remodeling of retinal circuits will be critical for the design of successful vision rescue strategies. Frontiers Media S.A. 2015-10-07 /pmc/articles/PMC4595653/ /pubmed/26500497 http://dx.doi.org/10.3389/fncel.2015.00395 Text en Copyright © 2015 Soto and Kerschensteiner. 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) or licensor 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 Neuroscience
Soto, Florentina
Kerschensteiner, Daniel
Synaptic remodeling of neuronal circuits in early retinal degeneration
title Synaptic remodeling of neuronal circuits in early retinal degeneration
title_full Synaptic remodeling of neuronal circuits in early retinal degeneration
title_fullStr Synaptic remodeling of neuronal circuits in early retinal degeneration
title_full_unstemmed Synaptic remodeling of neuronal circuits in early retinal degeneration
title_short Synaptic remodeling of neuronal circuits in early retinal degeneration
title_sort synaptic remodeling of neuronal circuits in early retinal degeneration
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4595653/
https://www.ncbi.nlm.nih.gov/pubmed/26500497
http://dx.doi.org/10.3389/fncel.2015.00395
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