Source:http://linkedlifedata.com/resource/pubmed/id/11050103
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2001-3-6
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pubmed:abstractText |
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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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
19
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pubmed:volume |
276
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1800-7
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11050103-Animals,
pubmed-meshheading:11050103-Calcium,
pubmed-meshheading:11050103-Cerebral Cortex,
pubmed-meshheading:11050103-Coculture Techniques,
pubmed-meshheading:11050103-Inositol 1,4,5-Trisphosphate,
pubmed-meshheading:11050103-Ion Transport,
pubmed-meshheading:11050103-Neuroglia,
pubmed-meshheading:11050103-Neurons,
pubmed-meshheading:11050103-Rats,
pubmed-meshheading:11050103-Rats, Sprague-Dawley,
pubmed-meshheading:11050103-Thapsigargin
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pubmed:year |
2001
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pubmed:articleTitle |
Traumatic injury of cortical neurons causes changes in intracellular calcium stores and capacitative calcium influx.
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pubmed:affiliation |
Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298-0613, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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