Interhemispheric plasticity is mediated by maximal potentiation of callosal inputs.
Animals
Brain
Corpus Callosum
/ physiology
Long-Term Potentiation
/ physiology
Magnetic Resonance Imaging
/ methods
Mice
Neuronal Plasticity
/ physiology
Neurons
/ physiology
Receptors, N-Methyl-D-Aspartate
Sensation
/ physiology
Sensory Deprivation
/ physiology
Somatosensory Cortex
/ physiology
Synapses
/ physiology
Vibrissae
/ physiology
corpus callosum
cortical circuit
interhemispheric plasticity
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
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
6391-6396Informations de copyright
Copyright © 2019 the Author(s). Published by PNAS.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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