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Influence of therapeutic hypothermia on neuroprotection and post-ischemic plasticity in a rat model of global ischemia Open Access


Other title
Type of item
Degree grantor
University of Alberta
Author or creator
Silasi, Gergely
Supervisor and department
Colbourne, Fred (Neuroscience)
Examining committee member and department
Treit, Dallas (Psychology)
Winship, Ian (Psychiatry)
Fouad, Karim (Rehab Medicine)
Walz, Wolfgang (Psychiatry)
Centre for Neuroscience

Date accepted
Graduation date
Doctor of Philosophy
Degree level
Blood flow to the brain may be disrupted by either a stroke (such as focal ischemia or hemorrhage) or cardiac arrest, where the whole brain becomes ischemic. Both forms of injury result in irreversible neuronal loss leading to neurological impairments and a decrease in the quality of life. Neuroprotective treatments are aimed at minimizing the damage that occurs after brain ischemia, and one of the most successful neuroprotectants developed so far is therapeutic hypothermia. Prolonged cooling has been shown to prevent CA1 neuronal death in animal models of global ischemia and the treatment also improves survival and neurological function in patients resuscitated from cardiac arrest. In contrast to the well know neuroprotective properties of hypothermia, the effect of this treatment on post-ischemic plasticity and reorganization has not been clearly investigated. This is an important issue, as plastic changes in remaining brain circuits facilitate functional improvement and recovery after ischemia. The current thesis evaluated the influence of hypothermia on several forms of post-ischemic plasticity including neurogenesis and growth factor expression in the hippocampus. A rat model of global ischemia was used to induce degeneration of hippocampal CA1 neurons, and hypothermia was applied either systemically (whole body cooling) or through unilateral brain cooling. We found that the treatment did not negatively impact post-ischemic plasticity on any of our measures even when cooling was maintained for up to 7 days. These results suggest that prolonged cooling may be a safe treatment, however additional models of ischemia should be used to assess this in future studies.
License granted by Gergely Silasi ( on 2011-06-28T05:00:10Z (GMT): Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of the above terms. The author reserves all other publication and other rights in association with the copyright in the thesis, and except as herein provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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