HAL (France)
open access
ATP1A3 dysfunction causes motor hyperexcitability and afterhyperpolarization loss in a dystonia model
Abstract Mutations in the gene encoding the alpha3 Na+/K+-ATPase isoform (ATP1A3) lead to movement disorders that manifest with dystonia, a common neurological symptom with many different origins, but for which the underlying molecular mechanisms remain poorly understood. We have generated an ATP1A3
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