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• W1607372012 abstract "Mutations in the enzyme superoxide dismutase 1 (SOD1) initiate a progressive motoneurone degeneration in amyotrophic lateral sclerosis (ALS). Transgenic mice overexpressing this mutation develop a similar progressive motoneurone degeneration. In spinal motoneurones cultured from presymptomatic mice expressing the glycine to alanine mutation at base pair 93 (G93A) SOD1 mutation, a marked increase in the persistent component of the Na + current was observed, without changes in passive properties. This increase only enhanced neuronal excitability in high input conductance cells, as low input conductance cells exhibited a compensatory outward shift in the current remaining after Na + blockade. High input conductance motoneurones tend to be large, so these results may explain the tendency of large motoneurones to degenerate first in ALS. Riluzole, at the therapeutic concentration used to treat ALS, decreased neuronal excitability and persistent Na + current in G93A motoneurones to levels observed in the control motoneurones. Aberrations in the intrinsic electrical properties may be among the first symptoms to emerge in SOD1‐linked ALS." @default.
• W1607372012 created "2016-06-24" @default.
• W1607372012 creator A5027270454 @default.
• W1607372012 creator A5050915751 @default.
• W1607372012 creator A5063753709 @default.
• W1607372012 creator A5080947810 @default.
• W1607372012 date "2005-03-01" @default.
• W1607372012 modified "2023-10-15" @default.
• W1607372012 title "Increased persistent Na⁺current and its effect on excitability in motoneurones cultured from mutant SOD1 mice" @default.
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• W1607372012 doi "https://doi.org/10.1113/jphysiol.2004.074138" @default.
• W1607372012 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1665614" @default.
• W1607372012 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15649979" @default.
• W1607372012 hasPublicationYear "2005" @default.
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