Interhemispheric plasticity is mediated by maximal potentiation of callosal inputs.


Journal

Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876

Informations de publication

Date de publication:
26 03 2019
Historique:
pubmed: 9 3 2019
medline: 21 5 2019
entrez: 9 3 2019
Statut: ppublish

Résumé

Central or peripheral injury causes reorganization of the brain's connections and functions. A striking change observed after unilateral stroke or amputation is a recruitment of bilateral cortical responses to sensation or movement of the unaffected peripheral area. The mechanisms underlying this phenomenon are described in a mouse model of unilateral whisker deprivation. Stimulation of intact whiskers yields a bilateral blood-oxygen-level-dependent fMRI response in somatosensory barrel cortex. Whole-cell electrophysiology demonstrated that the intact barrel cortex selectively strengthens callosal synapses to layer 5 neurons in the deprived cortex. These synapses have larger AMPA receptor- and NMDA receptor-mediated events. These factors contribute to a maximally potentiated callosal synapse. This potentiation occludes long-term potentiation, which could be rescued, to some extent, with prior long-term depression induction. Excitability and excitation/inhibition balance were altered in a manner consistent with cell-specific callosal changes and support a shift in the overall state of the cortex. This is a demonstration of a cell-specific, synaptic mechanism underlying interhemispheric cortical reorganization.

Identifiants

pubmed: 30846552
pii: 1810132116
doi: 10.1073/pnas.1810132116
pmc: PMC6442599
doi:

Substances chimiques

Receptors, N-Methyl-D-Aspartate 0

Types de publication

Journal Article Research Support, N.I.H., Intramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

6391-6396

Informations de copyright

Copyright © 2019 the Author(s). Published by PNAS.

Déclaration de conflit d'intérêts

The authors declare no conflict of interest.

Références

Neuron. 2014 Feb 5;81(3):664-73
pubmed: 24507197
Neuron. 2004 Sep 30;44(1):5-21
pubmed: 15450156
Cereb Cortex. 2011 Apr;21(4):756-68
pubmed: 20801897
Philos Trans R Soc Lond B Biol Sci. 2014 Oct 19;369(1654):20130601
pubmed: 25225095
Ann Neurol. 2008 Feb;63(2):236-46
pubmed: 17896791
Arch Neurol. 1971 Oct;25(4):302-6
pubmed: 5110123
Neuron. 2012 May 24;74(4):731-42
pubmed: 22632730
Nature. 1994 Mar 10;368(6467):144-7
pubmed: 8139656
Stroke. 1999 Nov;30(11):2331-40
pubmed: 10548667
Nat Neurosci. 2015 Nov;18(11):1687-1697
pubmed: 26457553
PLoS Comput Biol. 2015 Mar 13;11(3):e1004090
pubmed: 25768881
Cereb Cortex. 2017 Jul 1;27(7):3869-3878
pubmed: 28444185
Nat Neurosci. 2007 May;10(5):663-8
pubmed: 17435752
Cereb Cortex. 2002 Jan;12(1):86-97
pubmed: 11734535
Nature. 2001 May 31;411(6837):583-7
pubmed: 11385572
J Neurophysiol. 2000 May;83(5):2542-53
pubmed: 10805656
Neuron. 2009 Dec 10;64(5):707-18
pubmed: 20005826
Nat Neurosci. 1999 Apr;2(4):352-7
pubmed: 10204542
Neuroscience. 2002;111(4):761-73
pubmed: 12031403
Science. 2000 Oct 20;290(5491):533-6
pubmed: 11039938
J Physiol. 2018 May 15;596(10):1949-1964
pubmed: 29508394
J Neurosci. 2005 Jun 29;25(26):6221-34
pubmed: 15987952
Science. 1987 Jul 3;237(4810):42-8
pubmed: 3037696
Neuroimage. 2014 Nov 15;102 Pt 2:838-47
pubmed: 25175535
Nature. 1998 Feb 26;391(6670):892-6
pubmed: 9495341
Neuron. 2012 Feb 9;73(3):497-510
pubmed: 22325202
Exp Brain Res. 1992;88(1):33-40
pubmed: 1347272
Proc Natl Acad Sci U S A. 1994 Dec 20;91(26):12942-6
pubmed: 7809151
Neural Plast. 2012;2012:838672
pubmed: 22792494
Nat Rev Neurosci. 2006 Nov;7(11):873-81
pubmed: 17053811
J Neural Eng. 2018 Aug;15(4):046033
pubmed: 29855433
Brain Connect. 2014 Nov;4(9):709-17
pubmed: 25117691
Nature. 1997 Sep 11;389(6647):180-3
pubmed: 9296495
Neuroimage. 2012 Oct 1;62(4):2190-200
pubmed: 22040739
Neuroscientist. 2014 Feb;20(1):56-70
pubmed: 23774218
J Pain. 2016 Aug;17(8):911-8
pubmed: 27260638

Auteurs

Emily Petrus (E)

Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892; emily.petrus@nih.gov KoretskyA@ninds.nih.gov.

Galit Saar (G)

Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

Zhiwei Ma (Z)

Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

Steve Dodd (S)

Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

John T R Isaac (JTR)

Department of Physiology, University of Toronto, Toronto ON MS5 1A8, Canada.

Alan P Koretsky (AP)

Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892; emily.petrus@nih.gov KoretskyA@ninds.nih.gov.

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Classifications MeSH