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  The chloride transporter Na(+)-K(+)-Cl- cotransporter isoform-1 contributes to intracellular chloride increases after in vitro ischemia

Pond, B. B., Berglund, K., Kuner, T., Feng, G., Augustine, G. J., & Schwartz-Bloom, R. D. (2006). The chloride transporter Na(+)-K(+)-Cl- cotransporter isoform-1 contributes to intracellular chloride increases after in vitro ischemia. The Journal of Neuroscience: the Official Journal of the Society for Neuroscience, 26(5), 1396-1406. doi:10.1523/JNEUROSCI.1421-05.2006.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-EC9F-C Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-ECA0-6
Genre: Journal Article

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JNeurosci_26_2006_1396.pdf (Any fulltext), 888KB
 
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 Creators:
Pond, Brooks B., Author
Berglund, Ken, Author
Kuner, Thomas1, Author              
Feng, Guoping, Author
Augustine, George J., Author
Schwartz-Bloom, Rochelle D., Author
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1Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              

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Free keywords: oxygen-glucose deprivation; Na-K-Cl cotransporter; Clomeleon; bumetanide; furosemide; picrotoxin
 Abstract: Ischemic episodes in the CNS cause significant disturbances in neuronal ionic homeostasis. To directly measure changes in intracellular Cl- concentration ([Cl-]i) during and after ischemia, we used Clomeleon, a novel ratiometric optical indicator for Cl-. Hippocampal slices from adult transgenic mice expressing Clomeleon in hippocampal neurons were subjected to 8 min of oxygen-glucose deprivation (OGD) (an in vitro model for ischemia) and reoxygenated in the presence of glucose. This produced mild neuronal damage 3 h later that was prevented when the extracellular [Cl-] was maintained at 10 mm during reoxygenation. OGD induced a transient decrease in fluorescence resonance energy transfer within Clomeleon, indicating an increase in [Cl-]i. During reoxygenation, there was a partial recovery in [Cl-]i, but [Cl-]i rose again 45 min later. To investigate sources of Cl- accumulation, we examined the effects of Cl- transport inhibitors on the rises in [Cl-]i during and after OGD. Bumetanide and furosemide, which inhibit Cl- influx through the Na(+)-K(+)-Cl- cotransporter isoform-1 (NKCC-1) and efflux through the K(+)-Cl- cotransporter isoform-2, were unable to inhibit the first rise in [Cl-]i, yet entirely prevented the secondary rise in [Cl-]i during reoxygenation. In contrast, picrotoxin, which blocks the GABA-gated Cl- channel, did not inhibit the secondary rise in [Cl-]i after OGD. [Cl-]i increases during reoxygenation were accompanied by an increase in phosphorylation of NKCC-1, an indication of increased NKCC-1 activity after OGD. We conclude that NKCC-1 plays an important role in OGD-induced Cl- accumulation and subsequent neuronal damage.

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Language(s): eng - English
 Dates: 2005-12-102004-12-182005-12-122006-02-01
 Publication Status: Published in print
 Pages: 11
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 Table of Contents: -
 Rev. Type: Peer
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Title: The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
  Other : J. Neurosci.
Source Genre: Journal
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Publ. Info: Baltimore, MD : The Society
Pages: - Volume / Issue: 26 (5) Sequence Number: - Start / End Page: 1396 - 1406 Identifier: ISSN: 0270-6474
CoNE: https://pure.mpg.de/cone/journals/resource/954925502187_1