IndraLab

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SCN8A inhibits sodium(1+). 7 / 7
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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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"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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"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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"Downregulation of SCN8A (Scenario 2 in Figure 3C), which is enriched in excitatory neurons, could reduce the sodium entry to excitatory neurons and probably their excitability and may explain its protective effect.The inhibition of pyramidal neurons by PV and SST interneurons is widely acknowledged, and a decrease in their function has been observed in animal models of epilepsy [93,94]."
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"Deleting the SVA in SCN8A increases sodium currents (Fig. 4c) without altering resting membrane potential (Fig. 4d) or capacitance (Fig. 4e)."
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"36 Downregulation of the Scn8a gene has previously been shown to reduce sodium current in the rat sensory ganglionic cells and slow neuronal firing."
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"GS967, a potent and unconventional sodium channel blocker, is a Nav1.6 modulator that inhibits the persistent sodium current and exhibits a protective effect, which shows that a significantly improved survival of SCN1A+/- mice and suppressed spontaneous seizures by involving a secondary change in Nav1.6."
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