Abstract
It is now well established that the neurotransmitter glutamate plays a prominentrole in the pathogenesis of hypoxic-ischemic brain damage [1, 2] High levels of glutamate accumulate in the interstitial fluid during an ischemic/traumatic episode [3] and, through the activation of ionotropic glutamate receptors, initiate a cascade of cellular events which ultimately lead to irreversible cell damage. These cellular events contributing to excitotoxicity appear to be triggered largely by destabilization of calcium homeostasis [4].
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© 1994 Springer-Verlag Berlin Heidelberg
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Seren, M.S. et al. (1994). Monosialoganglioside GM1 in Experimental Models of Stroke. In: Hartmann, A., Yatsu, F., Kuschinsky, W. (eds) Cerebral Ischemia and Basic Mechanisms. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-78151-3_13
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DOI: https://doi.org/10.1007/978-3-642-78151-3_13
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-78153-7
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