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Oligodendrocyte-mediated myelin plasticity and its role in neural synchronization
Temporal synchrony of signals arriving from different neurons or brain regions is essential for proper neural processing. Nevertheless, it is not well understood how such synchrony is achieved and maintained in a complex network of time-delayed neural interactions. Myelin plasticity, accomplished by...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
eLife Sciences Publications, Ltd
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10132807/ https://www.ncbi.nlm.nih.gov/pubmed/36976252 http://dx.doi.org/10.7554/eLife.81982 |
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author | Pajevic, Sinisa Plenz, Dietmar Basser, Peter J Fields, R Douglas |
author_facet | Pajevic, Sinisa Plenz, Dietmar Basser, Peter J Fields, R Douglas |
author_sort | Pajevic, Sinisa |
collection | PubMed |
description | Temporal synchrony of signals arriving from different neurons or brain regions is essential for proper neural processing. Nevertheless, it is not well understood how such synchrony is achieved and maintained in a complex network of time-delayed neural interactions. Myelin plasticity, accomplished by oligodendrocytes (OLs), has been suggested as an efficient mechanism for controlling timing in brain communications through adaptive changes of axonal conduction velocity and consequently conduction time delays, or latencies; however, local rules and feedback mechanisms that OLs use to achieve synchronization are not known. We propose a mathematical model of oligodendrocyte-mediated myelin plasticity (OMP) in which OLs play an active role in providing such feedback. This is achieved without using arrival times at the synapse or modulatory signaling from astrocytes; instead, it relies on the presence of global and transient OL responses to local action potentials in the axons they myelinate. While inspired by OL morphology, we provide the theoretical underpinnings that motivated the model and explore its performance for a wide range of its parameters. Our results indicate that when the characteristic time of OL’s transient intracellular responses to neural spikes is between 10 and 40 ms and the firing rates in individual axons are relatively low (10 Hz), the OMP model efficiently synchronizes correlated and time-locked signals while latencies in axons carrying independent signals are unaffected. This suggests a novel form of selective synchronization in the CNS in which oligodendrocytes play an active role by modulating the conduction delays of correlated spike trains as they traverse to their targets. |
format | Online Article Text |
id | pubmed-10132807 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | eLife Sciences Publications, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-101328072023-04-27 Oligodendrocyte-mediated myelin plasticity and its role in neural synchronization Pajevic, Sinisa Plenz, Dietmar Basser, Peter J Fields, R Douglas eLife Neuroscience Temporal synchrony of signals arriving from different neurons or brain regions is essential for proper neural processing. Nevertheless, it is not well understood how such synchrony is achieved and maintained in a complex network of time-delayed neural interactions. Myelin plasticity, accomplished by oligodendrocytes (OLs), has been suggested as an efficient mechanism for controlling timing in brain communications through adaptive changes of axonal conduction velocity and consequently conduction time delays, or latencies; however, local rules and feedback mechanisms that OLs use to achieve synchronization are not known. We propose a mathematical model of oligodendrocyte-mediated myelin plasticity (OMP) in which OLs play an active role in providing such feedback. This is achieved without using arrival times at the synapse or modulatory signaling from astrocytes; instead, it relies on the presence of global and transient OL responses to local action potentials in the axons they myelinate. While inspired by OL morphology, we provide the theoretical underpinnings that motivated the model and explore its performance for a wide range of its parameters. Our results indicate that when the characteristic time of OL’s transient intracellular responses to neural spikes is between 10 and 40 ms and the firing rates in individual axons are relatively low (10 Hz), the OMP model efficiently synchronizes correlated and time-locked signals while latencies in axons carrying independent signals are unaffected. This suggests a novel form of selective synchronization in the CNS in which oligodendrocytes play an active role by modulating the conduction delays of correlated spike trains as they traverse to their targets. eLife Sciences Publications, Ltd 2023-03-28 /pmc/articles/PMC10132807/ /pubmed/36976252 http://dx.doi.org/10.7554/eLife.81982 Text en https://creativecommons.org/publicdomain/zero/1.0/This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication (https://creativecommons.org/publicdomain/zero/1.0/) . |
spellingShingle | Neuroscience Pajevic, Sinisa Plenz, Dietmar Basser, Peter J Fields, R Douglas Oligodendrocyte-mediated myelin plasticity and its role in neural synchronization |
title | Oligodendrocyte-mediated myelin plasticity and its role in neural synchronization |
title_full | Oligodendrocyte-mediated myelin plasticity and its role in neural synchronization |
title_fullStr | Oligodendrocyte-mediated myelin plasticity and its role in neural synchronization |
title_full_unstemmed | Oligodendrocyte-mediated myelin plasticity and its role in neural synchronization |
title_short | Oligodendrocyte-mediated myelin plasticity and its role in neural synchronization |
title_sort | oligodendrocyte-mediated myelin plasticity and its role in neural synchronization |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10132807/ https://www.ncbi.nlm.nih.gov/pubmed/36976252 http://dx.doi.org/10.7554/eLife.81982 |
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