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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:dateCreated |
1996-12-13
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| pubmed:abstractText |
1. We determined the intracellular Na+ concentration ([Na+]i) and mechanisms of its regulation in cultured rat hippocampal astrocytes using fluorescence ratio imaging of the Na+ indicator SBFI-AM (acetoxymethylester of sodium-binding benzofuran isophthalate, 10 microM). Dye signal calibration within the astrocytes showed that the ratiometric dye signal changed monotonically with changes in [Na+]i from 0 to 140 nM. The K+ sensitivity of the dye was negligible; intracellular pH changes, however, slightly affected the 'Na+' signal. 2. Baseline [Na+]i was 14.6 +/- 4.9 mM (mean +/- S.D.) in CO2/HCO3(-)-containing saline with 3 mM K+. Removal of extracellular Na+ decreased [Na+]i in two phases: a rapid phase of [Na+]i reduction (0.58 +/- 0.32 mM min-1) followed by a slower phase (0.15 +/- 0.09 mM min-1). 3. Changing from CO2/HCO3(-)-free to CO2/HCO3(-)-buffered saline resulted in a transient increase in [Na+]i of approximately 5 mM, suggesting activation of inward Na(+)-HCO3- cotransport by CO2/HCO3-. During furosemide (frusemide, 1 mM) or bumetanide (50 microM) application, a slow decrease in [Na+]i of approximately 2 mM was observed, indicating a steady inward transport of Na+ via Na(+)-K(+)-2Cl- cotransport under control conditions. Tetrodotoxin (100 microM) did not influence [Na+]i in the majority of cells (85%), suggesting that influx of Na+ through voltage-gated Na+ channels contributed to baseline [Na+]i in only a small subpopulation of hippocampal astrocytes. 4. Blocking Na+, K(+)-ATPase activity with cardiac glycosides (ouabain or strophanthidin, 1 mM) or removal of extracellular K+ led to an increase in [Na+]i of about 2 and 4 mM min-1, respectively. This indicated that Na+, K(+)-ATPase activity was critical in maintaining low [Na+]i in the face of a steep electrochemical gradient, which would favour a much higher [Na+]i. 5. Elevation of extracellular K+ concentration ([K+]o) by as little as 1 mM (from 3 to 4 mM) resulted in a rapid and reversible decrease in [Na+]i. Both the slope and the amplitude of the [K+]o-induced reductions in [Na+]i were sensitive to bumetanide. A reduction of [K+]o by 1 mM increased [Na+]i by 3.0 +/- 2.3 mM. In contrast, changing extracellular Na+ concentration by 20 mM resulted in changes in [Na+]i of less than 3 mM. 6. These results implied that in hippocampal astrocytes low baseline [Na+]i is determined by the action of Na(+)-HCO3- cotransport, Na(+)-K(+)-2Cl- cotransport and Na+, K(+)-ATPase, and that both Na+, K(+)-ATPase and inward Na(+)-K(+)-2Cl cotransport are activated by small, physiologically relevant increases in [K+]o. These mechanisms are well suited to help buffer increases in [K+]o associated with neural activity.
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| pubmed:grant | |
| pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-1348119,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-1375603,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-1614834,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-1712635,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-1761972,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-1869922,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-1999729,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-2169963,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-218691,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-2191780,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-2231783,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-2396701,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-2421839,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-2442359,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-2444257,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-2478559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-2479051,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-2808435,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-36128,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-3621030,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-4020694,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-4066764,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-4084790,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-6279427,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-6283023,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-6601260,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-6663651,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-6984493,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-7864922,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-7897475,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-7897491,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-8112821,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-8182422,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-832122,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-8367463,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8866855-8406681
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0022-3751
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
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| pubmed:volume |
491 ( Pt 2)
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
291-305
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| pubmed:dateRevised |
2009-11-18
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| pubmed:meshHeading | |
| pubmed:year |
1996
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| pubmed:articleTitle |
Intracellular sodium homeostasis in rat hippocampal astrocytes.
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| pubmed:affiliation |
Department of Neurology, Yale University School of Medicine, New Haven, CT 06520, 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
|