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  Progressive loss of a glial potassium channel (KCNJ10) in the spinal cord of the SOD1 (G93A) transgenic mouse model of amyotrophic lateral sclerosis

Kaiser, M., Maletzki, I., Hülsmann, S., Holtmann, B., Schulz-Schaeffer, W., Kirchhoff, F., et al. (2006). Progressive loss of a glial potassium channel (KCNJ10) in the spinal cord of the SOD1 (G93A) transgenic mouse model of amyotrophic lateral sclerosis. Journal of Neurochemistry, 99(3), 900-912. doi:10.1111/j.1471-4159.2006.04131.x.

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 Creators:
Kaiser, Melanie, Author
Maletzki, Iris, Author
Hülsmann, Swen, Author
Holtmann, Bettina, Author
Schulz-Schaeffer, Walter, Author
Kirchhoff, Frank1, Author           
Bähr, Mathias, Author
Neusch, Clemens, Author
Affiliations:
1Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173664              

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Free keywords: amyotrophic lateral sclerosis; glia; K+ buffering; KCNJ10; neurone-glia interaction; superoxide dismutase 1 transgenic mice MOTOR-NEURON DISEASE; CU/ZN SUPEROXIDE-DISMUTASE; TEMPORAL-LOBE EPILEPSY; GLUTAMATE TRANSPORTER; HIPPOCAMPAL SLICES; WATER TRANSPORT; PHENOTYPIC IMPACT; EXTRACELLULAR K+; MULLER CELLS; FAMILIAL ALS
 Abstract: Transgenic mice expressing the superoxide dismutase G93A mutation (SOD1(G93A)) were used to investigate the role of glial inwardly rectifying K+ (Kir)4.1 channels, which buffer extracellular K+ increases in response to neuronal excitation. A progressive decrease in Kir4.1 immunoreactivity was observed predominantly in the ventral horn of SOD1(G93A) mutants. Immunoblotting of spinal cord extracts mirrored these changes by showing a loss of Kir4.1 channels from presymptomatic stages onwards. Kir4.1 channels were found to be expressed in the spinal cord grey matter, targetting astrocytes and clustering around capillaries, supporting their role in clearance of extracellular K+. To understand the functional implications of extracellular K+ increases, we challenged the NSC34 motor neurone cell line with increasing extracellular K+ concentrations. Exposure to high extracellular K+ induced progressive motor neurone cell death. We suggest that loss of Kir4.1 impairs perineural K+ homeostasis and may contribute to motor neurone degeneration in SOD1(G93A) mutants by K+ excitotoxic mechanisms.

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Language(s): eng - English
 Dates: 2006-11
 Publication Status: Issued
 Pages: -
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 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 292142
ISI: 000241345100021
ISI: 000241345100021
DOI: 10.1111/j.1471-4159.2006.04131.x
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Title: Journal of Neurochemistry
  Alternative Title : J. Neurochem.
Source Genre: Journal
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Pages: - Volume / Issue: 99 (3) Sequence Number: - Start / End Page: 900 - 912 Identifier: ISSN: 0022-3042