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Network remodeling induced by transcranial brain stimulation: A computational model of tDCS-triggered cell assembly formation
Transcranial direct current stimulation (tDCS) is a variant of noninvasive neuromodulation, which promises treatment for brain diseases like major depressive disorder. In experiments, long-lasting aftereffects were observed, suggesting that persistent plastic changes are induced. The mechanism under...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MIT Press
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6777963/ https://www.ncbi.nlm.nih.gov/pubmed/31637332 http://dx.doi.org/10.1162/netn_a_00097 |
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author | Lu, Han Gallinaro, Júlia V. Rotter, Stefan |
author_facet | Lu, Han Gallinaro, Júlia V. Rotter, Stefan |
author_sort | Lu, Han |
collection | PubMed |
description | Transcranial direct current stimulation (tDCS) is a variant of noninvasive neuromodulation, which promises treatment for brain diseases like major depressive disorder. In experiments, long-lasting aftereffects were observed, suggesting that persistent plastic changes are induced. The mechanism underlying the emergence of lasting aftereffects, however, remains elusive. Here we propose a model, which assumes that tDCS triggers a homeostatic response of the network involving growth and decay of synapses. The cortical tissue exposed to tDCS is conceived as a recurrent network of excitatory and inhibitory neurons, with synapses subject to homeostatically regulated structural plasticity. We systematically tested various aspects of stimulation, including electrode size and montage, as well as stimulation intensity and duration. Our results suggest that transcranial stimulation perturbs the homeostatic equilibrium and leads to a pronounced growth response of the network. The stimulated population eventually eliminates excitatory synapses with the unstimulated population, and new synapses among stimulated neurons are grown to form a cell assembly. Strong focal stimulation tends to enhance the connectivity within new cell assemblies, and repetitive stimulation with well-chosen duty cycles can increase the impact of stimulation even further. One long-term goal of our work is to help in optimizing the use of tDCS in clinical applications. |
format | Online Article Text |
id | pubmed-6777963 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MIT Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-67779632019-10-21 Network remodeling induced by transcranial brain stimulation: A computational model of tDCS-triggered cell assembly formation Lu, Han Gallinaro, Júlia V. Rotter, Stefan Netw Neurosci Focus Feature: Linking Experimental and Computational Connectomics Transcranial direct current stimulation (tDCS) is a variant of noninvasive neuromodulation, which promises treatment for brain diseases like major depressive disorder. In experiments, long-lasting aftereffects were observed, suggesting that persistent plastic changes are induced. The mechanism underlying the emergence of lasting aftereffects, however, remains elusive. Here we propose a model, which assumes that tDCS triggers a homeostatic response of the network involving growth and decay of synapses. The cortical tissue exposed to tDCS is conceived as a recurrent network of excitatory and inhibitory neurons, with synapses subject to homeostatically regulated structural plasticity. We systematically tested various aspects of stimulation, including electrode size and montage, as well as stimulation intensity and duration. Our results suggest that transcranial stimulation perturbs the homeostatic equilibrium and leads to a pronounced growth response of the network. The stimulated population eventually eliminates excitatory synapses with the unstimulated population, and new synapses among stimulated neurons are grown to form a cell assembly. Strong focal stimulation tends to enhance the connectivity within new cell assemblies, and repetitive stimulation with well-chosen duty cycles can increase the impact of stimulation even further. One long-term goal of our work is to help in optimizing the use of tDCS in clinical applications. MIT Press 2019-09-01 /pmc/articles/PMC6777963/ /pubmed/31637332 http://dx.doi.org/10.1162/netn_a_00097 Text en © 2019 Massachusetts Institute of Technology This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. For a full description of the license, please visit https://creativecommons.org/licenses/by/4.0/legalcode. |
spellingShingle | Focus Feature: Linking Experimental and Computational Connectomics Lu, Han Gallinaro, Júlia V. Rotter, Stefan Network remodeling induced by transcranial brain stimulation: A computational model of tDCS-triggered cell assembly formation |
title | Network remodeling induced by transcranial brain stimulation: A computational model of tDCS-triggered cell assembly formation |
title_full | Network remodeling induced by transcranial brain stimulation: A computational model of tDCS-triggered cell assembly formation |
title_fullStr | Network remodeling induced by transcranial brain stimulation: A computational model of tDCS-triggered cell assembly formation |
title_full_unstemmed | Network remodeling induced by transcranial brain stimulation: A computational model of tDCS-triggered cell assembly formation |
title_short | Network remodeling induced by transcranial brain stimulation: A computational model of tDCS-triggered cell assembly formation |
title_sort | network remodeling induced by transcranial brain stimulation: a computational model of tdcs-triggered cell assembly formation |
topic | Focus Feature: Linking Experimental and Computational Connectomics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6777963/ https://www.ncbi.nlm.nih.gov/pubmed/31637332 http://dx.doi.org/10.1162/netn_a_00097 |
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