High potassium induces taurine release by osmosensitive and osmoresistant mechanisms in the rat hippocampus in vivo
The high potassium‐evoked taurine efflux in the nervous tissue has been entirely considered to be the result of the cell swelling produced by KCl influx via passive Donnan forces. However, the extracellular taurine increase evoked in the hippocampus by applying 6–100 mM KCl through microdialysis pro...
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Published in | Journal of neuroscience research Vol. 87; no. 1; pp. 208 - 217 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.01.2009
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Subjects | |
Online Access | Get full text |
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Summary: | The high potassium‐evoked taurine efflux in the nervous tissue has been entirely considered to be the result of the cell swelling produced by KCl influx via passive Donnan forces. However, the extracellular taurine increase evoked in the hippocampus by applying 6–100 mM KCl through microdialysis probes, which saturates at a concentration of 25 mM KCl, is not congruent with the mentioned osmosensitive release of taurine stimulated by high potassium. Therefore, we studied whether the taurine release elicited by different high KCl concentrations (25, 50, 75, or 100 mM) was blocked under hypertonic conditions (+100 mM sucrose). Taurine release stimulated by 25 mM KCl was totally osmosensitive, but that released by higher KCl concentrations became progressively osmoresistant, achieving more than the 60% of the extracellular taurine enhancement during 100 mM KCl perfusion. The osmoresistant taurine release evoked by 100 mM KCl perfusion was partially reduced by a solution without Ca2+ and with high Mg2+, or by D,L‐2‐amino‐5‐phosphopentanoic acid, an N‐methyl‐D‐aspartic acid (NMDA) receptor antagonist. Moreover, the release of taurine induced by a hypoosmotic solution was reduced by the presence ofeither high K+ (75 mM) or NMDA (100 μM). These results indicate that although moderately high [K+] evoke the osmosensitive release of taurine, higher [K+] inhibit it and trigger the release of taurine by an osmoresistant mechanism. This last component is partially mediated by NMDA receptors activated by the glutamate released during potassium‐induced depolarization. © 2008 Wiley‐Liss, Inc. |
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Bibliography: | istex:24412AEB1A4B02D81F4A44801BE67F012C173265 ark:/67375/WNG-K1VT83HG-B "Fondo de Investigaciones Sanitarias" - No. PI030615 ArticleID:JNR21818 The first two authors contributed equally to this work. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0360-4012 1097-4547 |
DOI: | 10.1002/jnr.21818 |