Post-traumatic seizures and changes in brain oxygen contribute to post-traumatic behavioural deficits.

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dc.contributor.advisorMychasiuk, Richelle M.
dc.contributor.advisorTeskey, G. Campbell
dc.contributor.authorMalik, Haris
dc.contributor.committeememberDunn, Jeff F.
dc.contributor.committeememberRho, Jong M.
dc.date2020-11
dc.date.accessioned2020-05-26T21:36:13Z
dc.date.available2020-05-26T21:36:13Z
dc.date.issued2020-05-22
dc.description.abstractRepetitive mild traumatic brain injuries (RmTBIs) are increasingly recognized to have long-term neurological sequelae in a significant proportion of patients. Individuals that have experienced RmTBIs exhibit a variety of physical, cognitive, or behavioural consequences that can negatively impact quality of life. Brain tissue oxygen levels are normally maintained through exquisite regulation of blood supply. However, during neurological events that result in alterations to brain tissue oxygen levels, neuronal dysfunction, brain damage (neuronal loss, astrocyte hypertrophy), and behavioural deficits have been observed, and are frequently related to poorer prognoses. The oxygenation response in the brain after mild TBIs or concussions have been poorly characterized, with most preliminary research limited to the cortex. Furthermore, the mechanisms by which traumatic brain injuries impact changes to brain oxygenation and vice versa remain unclear. In the current study we demonstrate that upon receiving RmTBIs, rats exhibit post-traumatic, electrographic, seizures that are accompanied by a long-lasting period of hippocampal hyperoxygenation. These seizures and the ensuing hyperoxic episodes are associated with deficits in working memory and motor coordination that are reversible through attenuation of the hyperoxia via administration of a calcium channel agonist, Bay K8644. We propose that the post-traumatic, postictal period of altered brain oxygenation is the basis for some of the common symptoms associated with mTBIs.en_US
dc.identifier.citationMalik, H. (2020). Post-traumatic seizures and changes in brain oxygen contribute to post-traumatic behavioural deficits. (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca.en_US
dc.identifier.doihttp://dx.doi.org/10.11575/PRISM/37883
dc.identifier.urihttp://hdl.handle.net/1880/112123
dc.language.isoengen_US
dc.publisher.facultyCumming School of Medicineen_US
dc.publisher.institutionUniversity of Calgaryen
dc.rightsUniversity of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission.en_US
dc.subjectConcussionen_US
dc.subjectseizureen_US
dc.subjectbrainen_US
dc.subjectoxygenationen_US
dc.subjectpost-traumatic deficitsen_US
dc.subjectmTBIen_US
dc.subjectbehaviouren_US
dc.subjectsymptomsen_US
dc.subject.classificationBiologyen_US
dc.subject.classificationNeuroscienceen_US
dc.subject.classificationPsychology--Behavioralen_US
dc.titlePost-traumatic seizures and changes in brain oxygen contribute to post-traumatic behavioural deficits.en_US
dc.typemaster thesisen_US
thesis.degree.disciplineMedicine – Neuroscienceen_US
thesis.degree.grantorUniversity of Calgaryen_US
thesis.degree.nameMaster of Science (MSc)en_US
ucalgary.item.requestcopytrueen_US
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