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Optimal compensation for neuron loss

The brain has an impressive ability to withstand neural damage. Diseases that kill neurons can go unnoticed for years, and incomplete brain lesions or silencing of neurons often fail to produce any behavioral effect. How does the brain compensate for such damage, and what are the limits of this comp...

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Detalles Bibliográficos
Autores principales: Barrett, David GT, Denève, Sophie, Machens, Christian K
Formato: Online Artículo Texto
Lenguaje:English
Publicado: eLife Sciences Publications, Ltd 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5283835/
https://www.ncbi.nlm.nih.gov/pubmed/27935480
http://dx.doi.org/10.7554/eLife.12454
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author Barrett, David GT
Denève, Sophie
Machens, Christian K
author_facet Barrett, David GT
Denève, Sophie
Machens, Christian K
author_sort Barrett, David GT
collection PubMed
description The brain has an impressive ability to withstand neural damage. Diseases that kill neurons can go unnoticed for years, and incomplete brain lesions or silencing of neurons often fail to produce any behavioral effect. How does the brain compensate for such damage, and what are the limits of this compensation? We propose that neural circuits instantly compensate for neuron loss, thereby preserving their function as much as possible. We show that this compensation can explain changes in tuning curves induced by neuron silencing across a variety of systems, including the primary visual cortex. We find that compensatory mechanisms can be implemented through the dynamics of networks with a tight balance of excitation and inhibition, without requiring synaptic plasticity. The limits of this compensatory mechanism are reached when excitation and inhibition become unbalanced, thereby demarcating a recovery boundary, where signal representation fails and where diseases may become symptomatic. DOI: http://dx.doi.org/10.7554/eLife.12454.001
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spelling pubmed-52838352017-02-02 Optimal compensation for neuron loss Barrett, David GT Denève, Sophie Machens, Christian K eLife Neuroscience The brain has an impressive ability to withstand neural damage. Diseases that kill neurons can go unnoticed for years, and incomplete brain lesions or silencing of neurons often fail to produce any behavioral effect. How does the brain compensate for such damage, and what are the limits of this compensation? We propose that neural circuits instantly compensate for neuron loss, thereby preserving their function as much as possible. We show that this compensation can explain changes in tuning curves induced by neuron silencing across a variety of systems, including the primary visual cortex. We find that compensatory mechanisms can be implemented through the dynamics of networks with a tight balance of excitation and inhibition, without requiring synaptic plasticity. The limits of this compensatory mechanism are reached when excitation and inhibition become unbalanced, thereby demarcating a recovery boundary, where signal representation fails and where diseases may become symptomatic. DOI: http://dx.doi.org/10.7554/eLife.12454.001 eLife Sciences Publications, Ltd 2016-12-09 /pmc/articles/PMC5283835/ /pubmed/27935480 http://dx.doi.org/10.7554/eLife.12454 Text en © 2016, Barrett et al https://creativecommons.org/licenses/by/4.0/This article is distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Neuroscience
Barrett, David GT
Denève, Sophie
Machens, Christian K
Optimal compensation for neuron loss
title Optimal compensation for neuron loss
title_full Optimal compensation for neuron loss
title_fullStr Optimal compensation for neuron loss
title_full_unstemmed Optimal compensation for neuron loss
title_short Optimal compensation for neuron loss
title_sort optimal compensation for neuron loss
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5283835/
https://www.ncbi.nlm.nih.gov/pubmed/27935480
http://dx.doi.org/10.7554/eLife.12454
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