Dyck, Richard H.Galasso, Sherri L.2017-12-182017-12-182007Galasso, S. L. (2007). Synaptic zinc and focal ischemic brain injury (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/1066http://hdl.handle.net/1880/102067Bibliography: p. 175-203Mounting evidence suggests that zinc, which can function both as a signalling mediator and a neurotoxin, is implicated in cerebral ischemia. To this effect, we investigated the specific role of synaptic vesicle zinc in acute focal ischemia by assessing the degree of intracellular zinc accumulation and neuronal degeneration in mice lacking synaptic zinc (ZnT-3 knockout). We found no significant differences in infarct volumes between adult male or female knockout, heterozygous, and wild-type mice. In addition, the time course of intracellular zinc accumulation was the same for all genotypes. Zinc was first detected at 6 hours and continued to be present for 2 weeks post-stroke. We conclude that intracellular zinc accumulation and cellular degeneration following focal ischemia occurs independent of the presence of synaptic zinc. As such, controlling the mobilization of zinc from intracellular stores may be more therapeutically advantageous than modulating synaptic zinc levels.xvii, 203 leaves : ill. ; 30 cm.engUniversity 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.master thesis10.11575/PRISM/1066