Source:http://linkedlifedata.com/resource/pubmed/id/14987443
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2004-2-27
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pubmed:abstractText |
Regulation of Ca2+ homeostasis in the extracellular space plays an important role in neuronal function. Several modeling studies and recent measurements have demonstrated that modest action potential or synaptic activity can result in a significant reduction in extracellular calcium ([Ca]o(2+)). Changes in [Ca]o(2+) can regulate intracellular signaling enzymes, such as Ca2+/calmodulin-dependent protein kinase II, and influence neuronal function at synaptic and nonsynaptic sites. The change in [Ca]o(2+) can affect several types of ion channels and neurotransmitter receptors and activate a Ca(2+)-sensitive receptor in neuronal membranes. Depletion of [Ca]o(2+) may function as an activity-dependent extracellular messenger that regulates nervous system function during development, learning, and disease.
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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 |
Feb
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pubmed:issn |
1073-8584
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
12-7
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading | |
pubmed:year |
2004
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pubmed:articleTitle |
Extracellular calcium depletion in synaptic transmission.
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pubmed:affiliation |
National Institutes of Health, National Institute for Child and Human Development, Section on Nervous System Development and Plasticity, Bethesda, MD 20892, USA.
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pubmed:publicationType |
Journal Article,
Review
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