Linked Life Data

11050103

Source:http://linkedlifedata.com/resource/pubmed/id/11050103

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pubmed-article:11050103pubmed:abstractTextUsing an in vitro traumatic injury model, we examined the effects of mechanical (stretch) injury on intracellular Ca2+ store-mediated signaling in cultured cortical neurons using fura-2. We previously found that elevation of [Ca2+](i) by the endoplasmic reticulum Ca2+-ATPase inhibitor, thapsigargin, was abolished 15 min post-injury. In the current studies, pre-injury inhibition of phospholipase C with neomycin sulfate maintained Ca2+-replete stores 15 min post-injury, suggesting that the initial injury-induced store depletion may be due to increased inositol trisphosphate production. Thapsigargin-stimulated elevation of [Ca2+](i) returned with time after injury and was potentiated at 3 h. Stimulation with thapsigargin in Ca2+-free media revealed that the size of the Ca2+ stores was normal at 3 h post-injury. However, Ca2+ influx triggered by depletion of intracellular Ca2+ stores (capacitative Ca2+ influx) was enhanced 3 h after injury. Enhancement was blocked by inhibitors of cytosolic phospholipase A2 and cytochrome P450 epoxygenase. Since intracellular Ca2+ store-mediated signaling plays an important role in neuronal function, the observed changes may contribute to dysfunction produced by traumatic brain injury. Additionally, our results suggest that capacitative Ca2+ influx may be mediated by both conformational coupling and a diffusible messenger synthesized by the combined action of cytosolic PLA2 and P450.lld:pubmed
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pubmed-article:11050103pubmed:authorpubmed-author:EllisE FEFlld:pubmed
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pubmed-article:11050103pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:11050103pubmed:articleTitleTraumatic injury of cortical neurons causes changes in intracellular calcium stores and capacitative calcium influx.lld:pubmed
pubmed-article:11050103pubmed:affiliationDepartment of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298-0613, USA.lld:pubmed
pubmed-article:11050103pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11050103pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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