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2015, Experimental NeurologyCitation Excerpt :Here, exogenous injection of 1 mM glutamate temporarily raised the extracellular glutamate concentration well beyond reported pathophysiologic values (~ 250 μM), but failed to produce significant neuronal damage. In contrast, SD can set the stage for excitotoxic lesion development since the massive ionic shifts of SD not only trigger glutamate release (Fabricius et al., 1993; Ueda et al., 1992; Zhou et al., 2013), but also remove the Mg2 + block from NMDARs and inhibit glutamate re-uptake by disrupting the electrochemical Na+ gradient that drives EAATs (Danbolt, 2001; Sarantis and Attwell, 1990; Szatkowski et al., 1990). The result is sustained activation of ionotropic glutamate receptors and calcium influx (Aiba and Shuttleworth, 2012; Zhou et al., 2013).
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