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Anoxic spreading depolarization in the neonatal rat cortex in vitro

Anoxic spreading depolarization (aSD) is a hallmark of ischemic injury in the cerebral cortex. In adults, aSD is associated with rapid and nearly complete neuronal depolarization and loss of neuronal functions. While ischemia also evokes aSD in the immature cortex, developmental aspects of neuronal...

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Autores principales: Gainutdinov, Azat, Juzekaeva, Elvira, Mukhtarov, Marat, Khazipov, Roustem
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10034194/
https://www.ncbi.nlm.nih.gov/pubmed/36970422
http://dx.doi.org/10.3389/fncel.2023.1106268
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author Gainutdinov, Azat
Juzekaeva, Elvira
Mukhtarov, Marat
Khazipov, Roustem
author_facet Gainutdinov, Azat
Juzekaeva, Elvira
Mukhtarov, Marat
Khazipov, Roustem
author_sort Gainutdinov, Azat
collection PubMed
description Anoxic spreading depolarization (aSD) is a hallmark of ischemic injury in the cerebral cortex. In adults, aSD is associated with rapid and nearly complete neuronal depolarization and loss of neuronal functions. While ischemia also evokes aSD in the immature cortex, developmental aspects of neuronal behavior during aSD remain largely unknown. Here, using oxygen-glucose deprivation (OGD) ischemia model in slices of the postnatal rat somatosensory cortex, we found that immature neurons displayed much more complex behaviors: they initially moderately depolarized during aSD, then transiently repolarised (for up to tens of minutes), and only then passed to terminal depolarization. The ability to fire action potentials was maintained in neurons mildly depolarized during aSD without reaching the level of depolarization block, and these functions were regained in the majority of immature neurons during post-aSD transient repolarization. The amplitude of depolarization and the probability of depolarization block during aSD increased, whereas transient post-SD repolarization levels and duration, and associated recovery in neuronal firing decreased with age. By the end of the first postnatal month, aSD acquired an adult-like phenotype, where depolarization during aSD merged with terminal depolarization and the phase of transient recovery was lost. Thus, changes in neuronal function during aSD undergo remarkable developmental changes that may contribute to lower susceptibility of the immature neurons to ischemia.
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spelling pubmed-100341942023-03-24 Anoxic spreading depolarization in the neonatal rat cortex in vitro Gainutdinov, Azat Juzekaeva, Elvira Mukhtarov, Marat Khazipov, Roustem Front Cell Neurosci Cellular Neuroscience Anoxic spreading depolarization (aSD) is a hallmark of ischemic injury in the cerebral cortex. In adults, aSD is associated with rapid and nearly complete neuronal depolarization and loss of neuronal functions. While ischemia also evokes aSD in the immature cortex, developmental aspects of neuronal behavior during aSD remain largely unknown. Here, using oxygen-glucose deprivation (OGD) ischemia model in slices of the postnatal rat somatosensory cortex, we found that immature neurons displayed much more complex behaviors: they initially moderately depolarized during aSD, then transiently repolarised (for up to tens of minutes), and only then passed to terminal depolarization. The ability to fire action potentials was maintained in neurons mildly depolarized during aSD without reaching the level of depolarization block, and these functions were regained in the majority of immature neurons during post-aSD transient repolarization. The amplitude of depolarization and the probability of depolarization block during aSD increased, whereas transient post-SD repolarization levels and duration, and associated recovery in neuronal firing decreased with age. By the end of the first postnatal month, aSD acquired an adult-like phenotype, where depolarization during aSD merged with terminal depolarization and the phase of transient recovery was lost. Thus, changes in neuronal function during aSD undergo remarkable developmental changes that may contribute to lower susceptibility of the immature neurons to ischemia. Frontiers Media S.A. 2023-03-09 /pmc/articles/PMC10034194/ /pubmed/36970422 http://dx.doi.org/10.3389/fncel.2023.1106268 Text en Copyright © 2023 Gainutdinov, Juzekaeva, Mukhtarov and Khazipov. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cellular Neuroscience
Gainutdinov, Azat
Juzekaeva, Elvira
Mukhtarov, Marat
Khazipov, Roustem
Anoxic spreading depolarization in the neonatal rat cortex in vitro
title Anoxic spreading depolarization in the neonatal rat cortex in vitro
title_full Anoxic spreading depolarization in the neonatal rat cortex in vitro
title_fullStr Anoxic spreading depolarization in the neonatal rat cortex in vitro
title_full_unstemmed Anoxic spreading depolarization in the neonatal rat cortex in vitro
title_short Anoxic spreading depolarization in the neonatal rat cortex in vitro
title_sort anoxic spreading depolarization in the neonatal rat cortex in vitro
topic Cellular Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10034194/
https://www.ncbi.nlm.nih.gov/pubmed/36970422
http://dx.doi.org/10.3389/fncel.2023.1106268
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