Sodium channel Na v1.6 is localized at nodes of Ranvier, dendrites, and synapses. The autism-associated gene Scn2a contributes to dendritic excitability and synaptic function in the prefrontal cortex. Nav1.1 localizes to axons of parvalbumin-positive inhibitory interneurons: a circuit basis for epileptic seizures in mice carrying an Scn1a gene mutation. Persistent Nav1.6 current at axon initial segments tunes spike timing of cerebellar granule cells. D1/D5 dopamine receptor activation differentially modulates rapidly inactivating and persistent sodium currents in prefrontal cortex pyramidal neurons. Maurice, N., Tkatch, T., Meisler, M., Sprunger, L. Role of sodium channel subtype in action potential generation by neocortical pyramidal neurons. Distinct contributions of Na v1.6 and Na v1.2 in action potential initiation and backpropagation. Nav1.6 sodium channels are critical to pacemaking and fast spiking in globus pallidus neurons. Impaired firing and cell-specific compensation in neurons lacking Na v1.6 sodium channels. Single-molecule imaging of Nav1.6 on the surface of hippocampal neurons reveals somatic nanoclusters. Preferential targeting of Nav1.6 voltage-gated Na + channels to the axon initial segment during development. Molecular identity of axonal sodium channels in human cortical pyramidal cells. Molecular identity of dendritic voltage-gated sodium channels. Distinct contributions of Nav1.6 and Nav1.2 in action potential initiation and backpropagation. Role of axonal NaV1.6 sodium channels in action potential initiation of CA1 pyramidal neurons. Polarized distribution of ion channels within microdomains of the axon initial segment. Functional specialization of the axon initial segment by isoform-specific sodium channel targeting. Comparative distribution of voltage-gated sodium channel proteins in human brain. The role of non-pore-forming beta subunits in physiology and pathophysiology of voltage-gated sodium channels. Electrophysiological properties of two axonal sodium channels, Nav1.2 and Nav1.6, expressed in mouse spinal sensory neurones. Functional analysis of the mouse Scn8a sodium channel. Variant-specific changes in persistent or resurgent sodium current in SCN8A-related epilepsy patient-derived neurons. Neuronal mechanisms of mutations in SCN8A causing epilepsy or intellectual disability. Distinct functional alterations in SCN8A epilepsy mutant channels. Altered subthreshold sodium currents and disrupted firing patterns in Purkinje neurons of Scn8a mutant mice. SCN3A-related neurodevelopmental disorder: a spectrum of epilepsy and brain malformation. Sodium channel SCN3A (NaV1.3) regulation of human cerebral cortical folding and oral motor development. Mutations in SCN3A cause early infantile epileptic encephalopathy. Voltage-gated sodium channel beta subunits and their related diseases. Sodium channel beta subunits: emerging targets in channelopathies. Diagnostic outcomes for genetic testing of 70 genes in 8565 patients with epilepsy and neurodevelopmental disorders. Adaptive evolution of voltage-gated sodium channels: the first 800 million years. A new look at an old question: when did the second whole genome duplication occur in vertebrate evolution? Genome Biol.
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