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J. Biol. Chem., Vol. 276, Issue 3, 1800-1807, January 19, 2001

This Article Full Text Full Text (PDF) All Versions of this Article: 276/3/1800    most recent M009209200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Weber, J. T. Articles by Ellis, E. F. Search for Related Content PubMed PubMed Citation Articles by Weber, J. T. Articles by Ellis, E. F. Social Bookmarking                      What's this?

Traumatic Injury of Cortical Neurons Causes Changes in Intracellular Calcium Stores and Capacitative Calcium Influx^*

John T. Weber, Beverly A. Rzigalinski, and Earl F. Ellis

From the Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298-0613

Using 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.

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