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          Institute: MPI für experimentelle Medizin     Collection: Neurogenetics     Display Documents



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ID: 292142.0, MPI für experimentelle Medizin / Neurogenetics
Progressive loss of a glial potassium channel (KCNJ10) in the spinal cord of the SOD1 (G93A) transgenic mouse model of amyotrophic lateral sclerosis
Authors:Kaiser, Melanie; Maletzki, Iris; Hülsmann, Swen; Holtmann, Bettina; Schulz-Schaeffer, Walter; Kirchhoff, Frank; Bähr, Mathias; Neusch, Clemens
Language:English
Date of Publication (YYYY-MM-DD):2006-11
Title of Journal:Journal of Neurochemistry
Journal Abbrev.:J. Neurochem.
Volume:99
Issue / Number:3
Start Page:900
End Page:912
Review Status:Peer-review
Audience:Experts Only
Abstract / Description: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.
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
External Publication Status:published
Document Type:Article
Communicated by:Klaus-Armin Nave
Affiliations:MPI für experimentelle Medizin/Neurogenetics
Relations:Has References-DOI:10.1111/j.1471-4159.2006.04131.x
Identifiers:ISSN:0022-3042 [ID No:1]
ISI:000241345100021 [ID No:2]
ISI:000241345100021 [ID No:3]
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