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Novel concepts in excitotoxic neurodegeneration after stroke

Published online by Cambridge University Press:  13 February 2004

Michelle M. Aarts
Affiliation:
Division of Cellular and Molecular Biology, Toronto Western Research Institute, Toronto Western Hospital, Suite 4W-435, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada.
Mark Arundine
Affiliation:
Division of Cellular and Molecular Biology, Toronto Western Research Institute, Toronto Western Hospital, Suite 4W-435, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada.
Michael Tymianski
Affiliation:
Division of Cellular and Molecular Biology, Toronto Western Research Institute, Toronto Western Hospital, Suite 4W-435, 399 Bathurst Street, Toronto, ON, M5T 2S8, Canada.
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Abstract

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Brain injury following cerebral ischaemia (stroke) involves a complex combination of pathological processes, including excitotoxicity and inflammation leading to necrotic and apoptotic forms of cell death. At the cellular level, excitotoxicity is mediated by glutamate and its cognate receptors, resulting in increased intracellular calcium and free radical production, and eventual cell death. Recent evidence suggests that scaffolding molecules that associate with glutamate receptors at the postsynaptic density allow coupling of receptor activity to specific second messengers capable of mediating excitotoxicity. These findings have important implications in the search for effective neuroprotective therapies in treating stroke.

Type
Review Article
Copyright
© Cambridge University Press 2003