Acute Post-Traumatic Sleep May Define Vulnerability to a Second Traumatic Brain Injury in Mice
AuthorRowe, Rachel K
Harrison, Jordan L
Morrison, Helena W
Murphy, Sean M
AffiliationUniv Arizona, Dept Child Hlth, Coll Med Phoenix
Univ Arizona, Dept Basic Med Sci, Coll Med Phoenix
Univ Arizona, Coll Nursing
Univ Arizona, Coll Engn
MetadataShow full item record
PublisherMARY ANN LIEBERT, INC
CitationRachel 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.2018.5980
JournalJOURNAL OF NEUROTRAUMA
RightsCopyright © 2019, Mary Ann Liebert, Inc., publishers
Collection InformationThis 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 firstname.lastname@example.org.
AbstractChronic 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.
Note12 month embargo; published online: 5 April 2019
VersionFinal accepted manuscript
SponsorsNational 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 Scholarship
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