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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MDPI AG
2021
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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) |
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cortical spreading depolarization electrocorticography traumatic brain injury brainstem oxidative stress Biology (General) QH301-705.5 Chemistry QD1-999 |
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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 |
work_keys_str_mv |
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