Optical imaging reveals cation-Cl- cotransporter-mediated transient rapid decrease in intracellular Cl- concentration induced by oxygen-glucose deprivation in rat neocortical slices

Citation
Y. Yamada et al., Optical imaging reveals cation-Cl- cotransporter-mediated transient rapid decrease in intracellular Cl- concentration induced by oxygen-glucose deprivation in rat neocortical slices, NEUROSCI RE, 39(3), 2001, pp. 269-280
Citations number
50
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROSCIENCE RESEARCH
ISSN journal
0168-0102 → ACNP
Volume
39
Issue
3
Year of publication
2001
Pages
269 - 280
Database
ISI
SICI code
0168-0102(200103)39:3<269:OIRCCT>2.0.ZU;2-L
Abstract
In brain slices from young (postnatal day (P) 10-15) rat somatosensory cort ex, real-time neuronal intracellular Cl- concentration ([C1-](i)) recording s were made by an optical technique measuring 6-methoxy-N-ethlquinolinium i odide (MEQ) fluorescence. Oxygen-glucose deprivation tin vitro model of isc hemia) induced a long-lasting [C1-]i increase preceded by a rapid, transien t [Cl-](i) decrease that could not be inhibited by blockers of Cl- pumps, C l- channels, or Cl- antiporters, but was sensitive to cation-Cl- cotranspor ter inhibitors (bumetanide and furosemide). Use of low external Na+ or high external K+ revealed that the Na+,K+-2Cl(-) cotransporter was inhibited by bumetanide and furosemide, whereas the K+-Cl- cotransporter was preferenti ally inhibited by furosemide under our experimental conditions. With a redu ced inward driving force for Na+ (reducing Na+,K+-2Cl(-) cotransport), the transient [Cl-](i) decrease was only rarely induced by oxygen-glucose depri vation. In contrast, with a reduced outward driving force for K+ (reducing K+-Cl- cotransport), the transient [Cl-](i) decrease still occurred. These results suggest that the transient [C1-]i decrease was primarily mediated b y a rapid inhibition of the inwardly directed Na+,K+ -2Cl(-) cotransporter. Reverse transcriptase-polymerase chain reaction (RT-PCR) experiments sugge sted that the isoform involved is NKCCl. We hypothesize that the initial ra pid C1- efflux might effectively delay the irreversible C1- influx that med iates neuronal injury. (C) 2001 Elsevier Science Ireland Ltd and the Japan Neuroscience Society. All rights reserved.