Synaptic zinc and focal ischemic brain injury
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2007
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Abstract
Mounting 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.
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Bibliography: p. 175-203
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Citation
Galasso, 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/1066