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Against cortical reorganisation
Neurological insults, such as congenital blindness, deafness, amputation, and stroke, often result in surprising and impressive behavioural changes. Cortical reorganisation, which refers to preserved brain tissue taking on a new functional role, is often invoked to account for these behavioural chan...
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/PMC10662956/ https://www.ncbi.nlm.nih.gov/pubmed/37986628 http://dx.doi.org/10.7554/eLife.84716 |
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author | Makin, Tamar R Krakauer, John W |
author_facet | Makin, Tamar R Krakauer, John W |
author_sort | Makin, Tamar R |
collection | PubMed |
description | Neurological insults, such as congenital blindness, deafness, amputation, and stroke, often result in surprising and impressive behavioural changes. Cortical reorganisation, which refers to preserved brain tissue taking on a new functional role, is often invoked to account for these behavioural changes. Here, we revisit many of the classical animal and patient cortical remapping studies that spawned this notion of reorganisation. We highlight empirical, methodological, and conceptual problems that call this notion into doubt. We argue that appeal to the idea of reorganisation is attributable in part to the way that cortical maps are empirically derived. Specifically, cortical maps are often defined based on oversimplified assumptions of ‘winner-takes-all’, which in turn leads to an erroneous interpretation of what it means when these maps appear to change. Conceptually, remapping is interpreted as a circuit receiving novel input and processing it in a way unrelated to its original function. This implies that neurons are either pluripotent enough to change what they are tuned to or that a circuit can change what it computes. Instead of reorganisation, we argue that remapping is more likely to occur due to potentiation of pre-existing architecture that already has the requisite representational and computational capacity pre-injury. This architecture can be facilitated via Hebbian and homeostatic plasticity mechanisms. Crucially, our revised framework proposes that opportunities for functional change are constrained throughout the lifespan by the underlying structural ‘blueprint’. At no period, including early in development, does the cortex offer structural opportunities for functional pluripotency. We conclude that reorganisation as a distinct form of cortical plasticity, ubiquitously evoked with words such as ‘take-over’’ and ‘rewiring’, does not exist. |
format | Online Article Text |
id | pubmed-10662956 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | eLife Sciences Publications, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-106629562023-11-21 Against cortical reorganisation Makin, Tamar R Krakauer, John W eLife Neuroscience Neurological insults, such as congenital blindness, deafness, amputation, and stroke, often result in surprising and impressive behavioural changes. Cortical reorganisation, which refers to preserved brain tissue taking on a new functional role, is often invoked to account for these behavioural changes. Here, we revisit many of the classical animal and patient cortical remapping studies that spawned this notion of reorganisation. We highlight empirical, methodological, and conceptual problems that call this notion into doubt. We argue that appeal to the idea of reorganisation is attributable in part to the way that cortical maps are empirically derived. Specifically, cortical maps are often defined based on oversimplified assumptions of ‘winner-takes-all’, which in turn leads to an erroneous interpretation of what it means when these maps appear to change. Conceptually, remapping is interpreted as a circuit receiving novel input and processing it in a way unrelated to its original function. This implies that neurons are either pluripotent enough to change what they are tuned to or that a circuit can change what it computes. Instead of reorganisation, we argue that remapping is more likely to occur due to potentiation of pre-existing architecture that already has the requisite representational and computational capacity pre-injury. This architecture can be facilitated via Hebbian and homeostatic plasticity mechanisms. Crucially, our revised framework proposes that opportunities for functional change are constrained throughout the lifespan by the underlying structural ‘blueprint’. At no period, including early in development, does the cortex offer structural opportunities for functional pluripotency. We conclude that reorganisation as a distinct form of cortical plasticity, ubiquitously evoked with words such as ‘take-over’’ and ‘rewiring’, does not exist. eLife Sciences Publications, Ltd 2023-11-21 /pmc/articles/PMC10662956/ /pubmed/37986628 http://dx.doi.org/10.7554/eLife.84716 Text en © 2023, Makin and Krakauer 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 Makin, Tamar R Krakauer, John W Against cortical reorganisation |
title | Against cortical reorganisation |
title_full | Against cortical reorganisation |
title_fullStr | Against cortical reorganisation |
title_full_unstemmed | Against cortical reorganisation |
title_short | Against cortical reorganisation |
title_sort | against cortical reorganisation |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10662956/ https://www.ncbi.nlm.nih.gov/pubmed/37986628 http://dx.doi.org/10.7554/eLife.84716 |
work_keys_str_mv | AT makintamarr againstcorticalreorganisation AT krakauerjohnw againstcorticalreorganisation |