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pubmed-article:10668567pubmed:abstractTextCalcium influx and elevation of intracellular free calcium ([Ca2+]i), with subsequent activation of degradative enzymes, is hypothesized to cause cell injury and death after traumatic brain injury. We examined the effects of mild-to-severe stretch-induced traumatic injury on [Ca2+]i dynamics in cortical neurons cultured on silastic membranes. [Ca2+]i was rapidly elevated after injury, however, the increase was transient with neuronal [Ca2+]i returning to basal levels by 3 h after injury, except in the most severely injured cells. Despite a return of [Ca2+]i to basal levels, there were persistent alterations in calcium-mediated signal transduction through 24 h after injury. [Ca2+]i elevation in response to glutamate or NMDA was enhanced after injury. We also found novel alterations in intracellular calcium store-mediated signaling. Neuronal calcium stores failed to respond to a stimulus 15 min after injury and exhibited potentiated responses to stimuli at 3 and 24 h post-injury. Thus, changes in calcium-mediated cellular signaling may contribute to the pathology that is observed after traumatic brain injury.lld:pubmed
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pubmed-article:10668567pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:10668567pubmed:articleTitleAlterations in calcium-mediated signal transduction after traumatic injury of cortical neurons.lld:pubmed
pubmed-article:10668567pubmed:affiliationDepartment of Pharmacology and Toxicology, Medical College of Virginia of Virginia Commonwealth University, Richmond, USA.lld:pubmed
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