| pubmed-article:9262234 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9262234 | lifeskim:mentions | umls-concept:C0206117 | lld:lifeskim |
| pubmed-article:9262234 | lifeskim:mentions | umls-concept:C0004112 | lld:lifeskim |
| pubmed-article:9262234 | lifeskim:mentions | umls-concept:C0086045 | lld:lifeskim |
| pubmed-article:9262234 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
| pubmed-article:9262234 | lifeskim:mentions | umls-concept:C0597484 | lld:lifeskim |
| pubmed-article:9262234 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:9262234 | pubmed:dateCreated | 1997-9-26 | lld:pubmed |
| pubmed-article:9262234 | pubmed:abstractText | Gap junctions between glial cells allow intercellular exchange of ions and small molecules. We have investigated the influence of gap junction coupling on regulation of intracellular Na+ concentration ([Na+]i) in cultured rat hippocampal astrocytes, using fluorescence ratio imaging with the Na+ indicator dye SBFI (sodium-binding benzofuran isophthalate). The [Na+]i in neighboring astrocytes was very similar (12.0 +/- 3.3 mM) and did not fluctuate under resting conditions. During uncoupling of gap junctions with octanol (0.5 mM), baseline [Na+]i was unaltered in 24%, increased in 54%, and decreased in 22% of cells. Qualitatively similar results were obtained with two other uncoupling agents, heptanol and alpha-glycyrrhetinic acid (AGA). Octanol did not alter the recovery from intracellular Na+ load induced by removal of extracellular K+, indicating that octanol's effects on baseline [Na+]i were not due to inhibition of Na+, K+-ATPase activity. Under control conditions, increasing [K+]o from 3 to 8 mM caused similar decreases in [Na+]i in groups of astrocytes, presumably by stimulating Na+, K+-ATPase. During octanol application, [K+]o-induced [Na+]i decreases were amplified in cells with increased baseline [Na+]i, and reduced in cells with decreased baseline [Na+]i. This suggests that baseline [Na+]i in astrocytes "sets" the responsiveness of Na+, K+-ATPase to increases in [K]o. Our results indicate that individual hippocampal astrocytes in culture rapidly develop different levels of baseline [Na+]i when they are isolated from one another by uncoupling agents. In astrocytes, therefore, an apparent function of coupling is the intercellular exchange of Na+ ions to equalize baseline [Na+]i, which serves to coordinate physiological responses that depend on the intracellular concentration of this ion. | lld:pubmed |
| pubmed-article:9262234 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9262234 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9262234 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9262234 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9262234 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:9262234 | pubmed:issn | 0894-1491 | lld:pubmed |
| pubmed-article:9262234 | pubmed:author | pubmed-author:RansomB RBR | lld:pubmed |
| pubmed-article:9262234 | pubmed:author | pubmed-author:RoseC RCR | lld:pubmed |
| pubmed-article:9262234 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9262234 | pubmed:volume | 20 | lld:pubmed |
| pubmed-article:9262234 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9262234 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9262234 | pubmed:pagination | 299-307 | lld:pubmed |
| pubmed-article:9262234 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:9262234 | pubmed:meshHeading | pubmed-meshheading:9262234-... | lld:pubmed |
| pubmed-article:9262234 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9262234 | pubmed:articleTitle | Gap junctions equalize intracellular Na+ concentration in astrocytes. | lld:pubmed |
| pubmed-article:9262234 | pubmed:affiliation | Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. crose@biomed.med.yale.edu | lld:pubmed |
| pubmed-article:9262234 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9262234 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9262234 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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