Acute Astrogliosis and neurological deficits following repeated mild traumatic brain injury

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dc.contributor.authorClarkson, Melissa A.
dc.contributor.supervisorChristie, Brian R.
dc.contributor.supervisorNahirney, Patrick C.
dc.date.accessioned2018-09-04T19:11:20Z
dc.date.available2018-09-04T19:11:20Z
dc.date.copyright2018en_US
dc.date.issued2018-09-04
dc.degree.departmentProgram: Neuroscienceen_US
dc.degree.levelMaster of Science M.Sc.en_US
dc.description.abstractMild traumatic brain injury (mTBI), often referred to as concussion, has become increasingly recognized as a serious health issue in the general population. The prevalence of mTBI in athletes, particularly repeated injuries in young athletes, is of great concern as injuries to the developing brain can have long-term detrimental effects. In this study we used a novel awake closed-head injury (ACHI) model in rodents to examine repeated mTBI (rmTBI), to determine if repeated injuries produced the neurological and molecular changes evident with human concussion. Animals were administered 4, 8, and 16 rmTBIs and acute neurological assessments were performed after the injuries. Changes in glial fibrillary acidic protein (GFAP) and ionized calcium-binding adapter molecule 1 (Iba-1) levels were assessed using Western blot analysis at one day following rmTBI in the ipsilateral dentate gyrus (DG) and the cornu ammonis (CA) regions of the hippocampus and the cortex (CX) indicative of astrocyte and microglial cell reactivity. Results indicated that the ACHI model produces neurological deficits immediately after the injuries, with the most deficits arising in the rmTBI16 group. Despite deficits in all injury groups, histological staining with cresyl violet revealed no significant morphological tissue damage to the brain. Western blot analysis, however, showed a significant increase in DG and CX GFAP expression in the rmTBI16 group with no changes in Iba-1 levels. This suggests an acute activation of astrocytes in response to injury, with a delay or absence of microglial activation. Our findings show that with repetitive concussions, we are able to detect acute neurological and molecular changes in the juvenile female brain. However, further investigation is necessary to determine if these are transient changes.en_US
dc.description.scholarlevelGraduateen_US
dc.identifier.bibliographicCitationMeconi, A., et al. (2018). Repeated mild traumatic brain injury can cause acute neurologic impairment without overt structural damage in juvenile rats. PLoS ONE, 13(5), 1–24.en_US
dc.identifier.urihttp://hdl.handle.net/1828/10027
dc.languageEnglisheng
dc.language.isoenen_US
dc.rightsAvailable to the World Wide Weben_US
dc.subjectMild Traumatic Brain Injuryen_US
dc.subjectAstrocytesen_US
dc.subjectMicrogliaen_US
dc.subjectConcussionen_US
dc.subjectHippocampusen_US
dc.subjectJuvenileen_US
dc.subjectGlial Fibrillary Acidic Proteinen_US
dc.subjectIonized calcium binding adapter molecule 1en_US
dc.subjectWestern Bloten_US
dc.subjectDentate Gyrusen_US
dc.subjectCornu Ammonisen_US
dc.subjectAwake Closed-Head Injuryen_US
dc.subjectFemaleen_US
dc.subjectNeuroinflammationen_US
dc.subjectCresyl Violeten_US
dc.subjectTraumatic Brain Injuryen_US
dc.subjectAstrogliosisen_US
dc.titleAcute Astrogliosis and neurological deficits following repeated mild traumatic brain injuryen_US
dc.typeThesisen_US

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