Brainstem and Cortical Spreading Depolarization in a Closed Head Injury Rat Model

Traumatic brain injury (TBI) is the leading cause of death in young individuals, and is a major health concern that often leads to long-lasting complications. However, the electrophysiological events that occur immediately after traumatic brain injury, and may underlie impact outcomes, have not been...

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Autores principales: Refat Aboghazleh, Ellen Parker, Lynn T. Yang, Daniela Kaufer, Jens P. Dreier, Alon Friedman, Gerben van Hameren
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Lenguaje:EN
Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/ce28ac93e49845de9804e2c2d9235a05
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spelling oai:doaj.org-article:ce28ac93e49845de9804e2c2d9235a052021-11-11T17:06:57ZBrainstem and Cortical Spreading Depolarization in a Closed Head Injury Rat Model10.3390/ijms2221116421422-00671661-6596https://doaj.org/article/ce28ac93e49845de9804e2c2d9235a052021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11642https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Traumatic brain injury (TBI) is the leading cause of death in young individuals, and is a major health concern that often leads to long-lasting complications. However, the electrophysiological events that occur immediately after traumatic brain injury, and may underlie impact outcomes, have not been fully elucidated. To investigate the electrophysiological events that immediately follow traumatic brain injury, a weight-drop model of traumatic brain injury was used in rats pre-implanted with epidural and intracerebral electrodes. Electrophysiological (near-direct current) recordings and simultaneous alternating current recordings of brain activity were started within seconds following impact. Cortical spreading depolarization (SD) and SD-induced spreading depression occurred in approximately 50% of mild and severe impacts. SD was recorded within three minutes after injury in either one or both brain hemispheres. Electrographic seizures were rare. While both TBI- and electrically induced SDs resulted in elevated oxidative stress, TBI-exposed brains showed a reduced antioxidant defense. In severe TBI, brainstem SD could be recorded in addition to cortical SD, but this did not lead to the death of the animals. Severe impact, however, led to immediate death in 24% of animals, and was electrocorticographically characterized by non-spreading depression (NSD) of activity followed by terminal SD in both cortex and brainstem.Refat AboghazlehEllen ParkerLynn T. YangDaniela KauferJens P. DreierAlon FriedmanGerben van HamerenMDPI AGarticlecortical spreading depolarizationelectrocorticographytraumatic brain injurybrainstemoxidative stressBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11642, p 11642 (2021)
institution DOAJ
collection DOAJ
language EN
topic cortical spreading depolarization
electrocorticography
traumatic brain injury
brainstem
oxidative stress
Biology (General)
QH301-705.5
Chemistry
QD1-999
spellingShingle cortical spreading depolarization
electrocorticography
traumatic brain injury
brainstem
oxidative stress
Biology (General)
QH301-705.5
Chemistry
QD1-999
Refat Aboghazleh
Ellen Parker
Lynn T. Yang
Daniela Kaufer
Jens P. Dreier
Alon Friedman
Gerben van Hameren
Brainstem and Cortical Spreading Depolarization in a Closed Head Injury Rat Model
description Traumatic brain injury (TBI) is the leading cause of death in young individuals, and is a major health concern that often leads to long-lasting complications. However, the electrophysiological events that occur immediately after traumatic brain injury, and may underlie impact outcomes, have not been fully elucidated. To investigate the electrophysiological events that immediately follow traumatic brain injury, a weight-drop model of traumatic brain injury was used in rats pre-implanted with epidural and intracerebral electrodes. Electrophysiological (near-direct current) recordings and simultaneous alternating current recordings of brain activity were started within seconds following impact. Cortical spreading depolarization (SD) and SD-induced spreading depression occurred in approximately 50% of mild and severe impacts. SD was recorded within three minutes after injury in either one or both brain hemispheres. Electrographic seizures were rare. While both TBI- and electrically induced SDs resulted in elevated oxidative stress, TBI-exposed brains showed a reduced antioxidant defense. In severe TBI, brainstem SD could be recorded in addition to cortical SD, but this did not lead to the death of the animals. Severe impact, however, led to immediate death in 24% of animals, and was electrocorticographically characterized by non-spreading depression (NSD) of activity followed by terminal SD in both cortex and brainstem.
format article
author Refat Aboghazleh
Ellen Parker
Lynn T. Yang
Daniela Kaufer
Jens P. Dreier
Alon Friedman
Gerben van Hameren
author_facet Refat Aboghazleh
Ellen Parker
Lynn T. Yang
Daniela Kaufer
Jens P. Dreier
Alon Friedman
Gerben van Hameren
author_sort Refat Aboghazleh
title Brainstem and Cortical Spreading Depolarization in a Closed Head Injury Rat Model
title_short Brainstem and Cortical Spreading Depolarization in a Closed Head Injury Rat Model
title_full Brainstem and Cortical Spreading Depolarization in a Closed Head Injury Rat Model
title_fullStr Brainstem and Cortical Spreading Depolarization in a Closed Head Injury Rat Model
title_full_unstemmed Brainstem and Cortical Spreading Depolarization in a Closed Head Injury Rat Model
title_sort brainstem and cortical spreading depolarization in a closed head injury rat model
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/ce28ac93e49845de9804e2c2d9235a05
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