Mediates the voltage-dependent sodium ion permeability of excitable membranes (PubMed:16921370, PubMed:17928448, PubMed:27281198). Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient. Plays a key role in brain, probably by regulating the moment when neurotransmitters are released in neurons (PubMed:16921370, PubMed:22914087). Involved in sensory perception of mechanical pain: activation in somatosensory neurons induces pain without neurogenic inflammation and produces hypersensitivity to mechanical, but not thermal stimuli (PubMed:27281198). Inactivation of this channel is specifically inhibited by the spider toxins Hm1a and Hm1b (H.maculata, AC P60992 and AC P0DOC5) in somatosensory neurons to elicit acute pain and mechanical allodynia (PubMed:27281198). The voltage-sensitive sodium channel consists of an ion conducting pore forming alpha-subunit regulated by one or more beta-1 (SCN1B), beta-2 (SCN2B), beta-3 (SCN3B) and/or beta-4 (SCN4B). Beta-1 (SCN1B) and beta-3 (SCN3B) are non-covalently associated with alpha, while beta-2 (SCN2B) and beta-4 (SCN4B) are covalently linked by disulfide bonds. Interacts with FGF13. Interacts with the conotoxin GVIIJ. Present in cerebellar Purkinje neurons (at protein level) (PubMed:17928448). Expressed by myelinated, non-C-fiber neurons in sensory ganglia (PubMed:27281198). The S3b-S4 and S1-S2 loops of repeat IV are targeted by H.maculata toxins Hm1a and Hm1b, leading to inhibit fast inactivation of Nav1.1/SCN1A. Selectivity for H.maculata toxins Hm1a and Hm1b depends on S1-S2 loops of repeat IV (PubMed:27281198). The sequence contains 4 internal repeats, each with 5 hydrophobic segments (S1, S2, S3, S5, S6) and one positively charged segment (S4). Segments S4 are probably the voltage-sensors and are characterized by a series of positively charged amino acids at every third position. Phosphorylation at Ser-1516 by PKC in a highly conserved cytoplasmic loop slows inactivation of the sodium channel and reduces peak sodium currents. Homozygous mice display severe seizures and premature death on postnatal day 15 (PubMed:16921370). Mice show severe motor deficits, including irregularity of stride length during locomotion, impaired motor reflexes in grasping and mild tremor in limbs when immobile, consistent with cerebellar dysfunction (PubMed:16921370). Heterozygous mice exhibit autistic-like behavior, characterized by hyperactivity, stereotyped behaviors, social interaction deficits and impaired context-dependent spatial memory (PubMed:22914087). Defects are caused by caused by impaired GABAergic neurotransmission (PubMed:22914087). Conditional knockout in forebrain GABAergic neurons leads to premature death caused by generalized tonic-clonic seizures in heterozygous mice (PubMed:22908258). Belongs to the sodium channel (TC 1.A.1.10) family. Nav1.1/SCN1A subfamily.