Linked Life Data

18338793

Source:http://linkedlifedata.com/resource/pubmed/id/18338793

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2008-4-28
pubmed:abstractText
Astrocytes can respond to a variety of stimuli by elevating their cytoplasmic Ca2+ concentration and can in turn release glutamate to signal adjacent neurons. The majority of this Ca2+ is derived from internal stores while a portion also comes from outside of the cell. Astrocytes use Ca2+ entry through store-operated Ca2+ channels to refill their internal stores. Therefore, we investigated what role this store-operated Ca2+ entry plays in astrocytic Ca2+ responses and subsequent glutamate release. Astrocytes express canonical transient receptor potential (TRPC) channels that have been implicated in mediating store-operated Ca2+ entry. Here, we show that astrocytes in culture and freshly isolated astrocytes from visual cortex express TRPC1, TRPC4, and TRPC5. Indirect immunocytochemistry reveals that these proteins are present throughout the cell; the predominant expression of functionally tested TRPC1, however, is on the plasma membrane. Labeling in freshly isolated astrocytes reveals changes in TRPC expression throughout development. Using an antibody against TRPC1 we were able to block the function of TRPC1 channels and determine their involvement in mechanically and agonist-evoked Ca2+ entry in cultured astrocytes. Blocking TRPC1 was also found to reduce mechanically induced Ca2+-dependent glutamate release. These data indicate that Ca2+ entry through TRPC1 channels contributes to Ca2+ signaling in astrocytes and the consequent glutamate release from these cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0894-1491
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2008 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
56
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
821-35
pubmed:meshHeading
pubmed-meshheading:18338793-Adenosine Triphosphate, pubmed-meshheading:18338793-Analysis of Variance, pubmed-meshheading:18338793-Animals, pubmed-meshheading:18338793-Animals, Newborn, pubmed-meshheading:18338793-Astrocytes, pubmed-meshheading:18338793-Calcium, pubmed-meshheading:18338793-Cells, Cultured, pubmed-meshheading:18338793-Enzyme Inhibitors, pubmed-meshheading:18338793-Glutamic Acid, pubmed-meshheading:18338793-Green Fluorescent Proteins, pubmed-meshheading:18338793-Indoles, pubmed-meshheading:18338793-Intracellular Fluid, pubmed-meshheading:18338793-Methoxyhydroxyphenylglycol, pubmed-meshheading:18338793-Nonlinear Dynamics, pubmed-meshheading:18338793-Physical Stimulation, pubmed-meshheading:18338793-Protein Transport, pubmed-meshheading:18338793-Rats, pubmed-meshheading:18338793-Rats, Sprague-Dawley, pubmed-meshheading:18338793-TRPC Cation Channels, pubmed-meshheading:18338793-Transfection, pubmed-meshheading:18338793-Visual Cortex
pubmed:year
2008
pubmed:articleTitle
Ca2+ entry through TRPC1 channels contributes to intracellular Ca2+ dynamics and consequent glutamate release from rat astrocytes.
pubmed:affiliation
Department of Neurobiology, Center for Glial Biology in Medicine, Atomic Force Microscopy and Nanotechnology Laboratories, Civitan International Research Center, Evelyn F. McKnight Brain Institute, University of Alabama, Birmingham, Alabama 35294, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural