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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Dove Medical Press
2015
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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) |
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Psychiatry RC435-571 Neurophysiology and neuropsychology QP351-495 |
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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 |
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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 |
work_keys_str_mv |
AT caronam sleepdeprivationdoesnotaffectneuronalsusceptibilitytomildtraumaticbraininjuryintherat AT stephensonr sleepdeprivationdoesnotaffectneuronalsusceptibilitytomildtraumaticbraininjuryintherat |
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