Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat

Aimee M Caron, Richard Stephenson Department of Cell and Systems Biology, University of Toronto, Toronto, ON, Canada Abstract: Mild and moderate traumatic brain injuries (TBIs) (and concussion) occur frequently as a result of falls, automobile accidents, and sporting activities, and are a major cau...

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Autores principales: Caron AM, Stephenson R
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Lenguaje:EN
Publicado: Dove Medical Press 2015
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spelling oai:doaj.org-article:e62f28433cda41e2bb1ee88f8b20b4042021-12-02T01:16:09ZSleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat1179-1608https://doaj.org/article/e62f28433cda41e2bb1ee88f8b20b4042015-06-01T00:00:00Zhttp://www.dovepress.com/sleep-deprivation-does-not-affect-neuronal-susceptibility-to-mild-trau-peer-reviewed-article-NSShttps://doaj.org/toc/1179-1608Aimee M Caron, Richard Stephenson Department of Cell and Systems Biology, University of Toronto, Toronto, ON, Canada Abstract: Mild and moderate traumatic brain injuries (TBIs) (and concussion) occur frequently as a result of falls, automobile accidents, and sporting activities, and are a major cause of acute and chronic disability. Fatigue and excessive sleepiness are associated with increased risk of accidents, but it is unknown whether prior sleep debt also affects the pathophysiological outcome of concussive injury. Using the “dark neuron” (DN) as a marker of reversible neuronal damage, we tested the hypothesis that acute (48 hours) total sleep deprivation (TSD) and chronic sleep restriction (CSR; 10 days, 6-hour sleep/day) affect DN formation following mild TBI in the rat. TSD and CSR were administered using a walking wheel apparatus. Mild TBI was administered under anesthesia using a weight-drop impact model, and the acute neuronal response was observed without recovery. DNs were detected using standard bright-field microscopy with toluidine blue stain following appropriate tissue fixation. DN density was low under home cage and sleep deprivation control conditions (respective median DN densities, 0.14% and 0.22% of neurons), and this was unaffected by TSD alone (0.1%). Mild TBI caused significantly higher DN densities (0.76%), and this was unchanged by preexisting acute or chronic sleep debt (TSD, 0.23%; CSR, 0.7%). Thus, although sleep debt may be predicted to increase the incidence of concussive injury, the present data suggest that sleep debt does not exacerbate the resulting neuronal damage. Keywords: sleep deprivation, concussion, traumatic brain injury, dark neuron, neurodegeneration, rat cortexCaron AMStephenson RDove Medical PressarticlePsychiatryRC435-571Neurophysiology and neuropsychologyQP351-495ENNature and Science of Sleep, Vol 2015, Iss default, Pp 63-72 (2015)
institution DOAJ
collection DOAJ
language EN
topic Psychiatry
RC435-571
Neurophysiology and neuropsychology
QP351-495
spellingShingle Psychiatry
RC435-571
Neurophysiology and neuropsychology
QP351-495
Caron AM
Stephenson R
Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat
description Aimee M Caron, Richard Stephenson Department of Cell and Systems Biology, University of Toronto, Toronto, ON, Canada Abstract: Mild and moderate traumatic brain injuries (TBIs) (and concussion) occur frequently as a result of falls, automobile accidents, and sporting activities, and are a major cause of acute and chronic disability. Fatigue and excessive sleepiness are associated with increased risk of accidents, but it is unknown whether prior sleep debt also affects the pathophysiological outcome of concussive injury. Using the “dark neuron” (DN) as a marker of reversible neuronal damage, we tested the hypothesis that acute (48 hours) total sleep deprivation (TSD) and chronic sleep restriction (CSR; 10 days, 6-hour sleep/day) affect DN formation following mild TBI in the rat. TSD and CSR were administered using a walking wheel apparatus. Mild TBI was administered under anesthesia using a weight-drop impact model, and the acute neuronal response was observed without recovery. DNs were detected using standard bright-field microscopy with toluidine blue stain following appropriate tissue fixation. DN density was low under home cage and sleep deprivation control conditions (respective median DN densities, 0.14% and 0.22% of neurons), and this was unaffected by TSD alone (0.1%). Mild TBI caused significantly higher DN densities (0.76%), and this was unchanged by preexisting acute or chronic sleep debt (TSD, 0.23%; CSR, 0.7%). Thus, although sleep debt may be predicted to increase the incidence of concussive injury, the present data suggest that sleep debt does not exacerbate the resulting neuronal damage. Keywords: sleep deprivation, concussion, traumatic brain injury, dark neuron, neurodegeneration, rat cortex
format article
author Caron AM
Stephenson R
author_facet Caron AM
Stephenson R
author_sort Caron AM
title Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat
title_short Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat
title_full Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat
title_fullStr Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat
title_full_unstemmed Sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat
title_sort sleep deprivation does not affect neuronal susceptibility to mild traumatic brain injury in the rat
publisher Dove Medical Press
publishDate 2015
url https://doaj.org/article/e62f28433cda41e2bb1ee88f8b20b404
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