IndraLab

Statements

SCN8A inhibits sodium(1+). 3 / 3
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"However, the available mouse models of Scn8a dysfunction have reduced sodium currents, whereas the N1786D is a gain-of-function mutation with increased persistent current, and Celf4 deficiency is believed to result in increased Na v 1.6 expression at the axon initial segment and increased persistent current."
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"Lower levels of SCN1A, SCN2A, SCN3A, SCN4A and SCN8A expression have also been reported in heart and shown to contribute approximately 23% of the total functional sodium channels in mouse ventricular myocytes and 27% in human atrial myocytes, based on TTX sensitivity."
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"Our results highlight a key role of this VGSC in information processing in these sensory neurons.Methods: The Mes V neuronal model follows a conductance-based Hodgkin-Huxley formalism and incorporates a potassium leak current (Ileak), a slow 4-AP sensitive potassium current (IK), and the complex Nav1.6 VGSC with a fast/transient sodium current (INaT), a slowly inactivating persistent sodium current (INaP), and an unconventional resurgent sodium current (INaR)."
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