Acute Post-Traumatic Sleep May Define Vulnerability to a Second Traumatic Brain Injury in Mice
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RoweJNeurotrauma2018 Resubmission ...
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Final Accepted Manuscript
Author
Rowe, Rachel KHarrison, Jordan L
Morrison, Helena W
Subbian, Vignesh
Murphy, Sean M
Lifshitz, Jonathan
Affiliation
Univ Arizona, Dept Child Hlth, Coll Med PhoenixUniv Arizona, Dept Basic Med Sci, Coll Med Phoenix
Univ Arizona, Coll Nursing
Univ Arizona, Coll Engn
Issue Date
2019-04-15
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MARY ANN LIEBERT, INCCitation
Rachel K. Rowe, Jordan L. Harrison, Helena W. Morrison, Vignesh Subbian, Sean M. Murphy, and Jonathan Lifshitz. Journal of Neurotrauma. Apr 2019. ahead of print. http://doi.org/10.1089/neu.2018.5980Journal
JOURNAL OF NEUROTRAUMARights
Copyright © 2019, Mary Ann Liebert, Inc., publishers.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Chronic neurological impairments can manifest from repetitive traumatic brain injury (rTBI), particularly when subsequent injuries occur before the initial injury completely heals. Herein, we apply post-traumatic sleep as a physiological biomarker of vulnerability, hypothesizing that a second TBI during post-traumatic sleep worsens neurological and histological outcomes compared to one TBI or a second TBI after post-traumatic sleep subsides. Mice received sham or diffuse TBI by midline fluid percussion injury; brain-injured mice received one TBI or rTBIs at 3- or 9-h intervals. Over 40 h post-injury, injured mice slept more than shams. Functional assessments indicated lower latencies on rotarod and increased Neurological Severity Scores for mice with rTBIs within 3 h. Anxiety-like behaviors in the open field task were increased for mice with rTBIs at 3 h. Based on pixel density of silver accumulation, neuropathology was greater at 28 days post-injury (DPI) in rTBI groups than sham and single TBI. Cortical microglia morphology was quantified and mice receiving rTBI were de-ramified at 14 DPI compared to shams and mice receiving a single TBI, suggesting robust microglial response in rTBI groups. Orexin-A-positive cells were sustained in the lateral hypothalamus with no loss detected, indicating that loss of wake-promoting neurons did not contribute to post-traumatic sleep. Thus, duration of post-traumatic sleep is a period of vulnerability that results in exacerbated injury from rTBI. Monitoring individual post-traumatic sleep is a potential clinical tool for personalized TBI management, where regular sleep patterns may inform rehabilitative strategies and return-to-activity guidelines.Note
12 month embargo; published online: 5 April 2019ISSN
0897-7151PubMed ID
30398389Version
Final accepted manuscriptSponsors
National Institute of Neurological Disorders and Stroke of the NIH [R21 NS072611, RO1 NS-065052]; PCH Mission Support Funds; Diane and Bruce Halle Foundation; NIHUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [F31 NS-090921]; Science Foundation Arizona Bisgrove Scholarshipae974a485f413a2113503eed53cd6c53
10.1089/neu.2018.5980
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