In neocortex, Nav1.1 is expressed in neocortical pyramidal tract projection neurons and a minor subpopulation of cortico-cortical projection neurons in addition to its predominant expression in inhibitory neurons, while the majority of cortico-thalamic, cortico-striatal, and cortico-cortical neurons express Nav1.2.

NBI-921352 (formerly XEN901) is a precision medicine in development for individuals with SCN8A gain-of-function mutations causing SCN8A related epilepsy syndrome (SCN8A-RES), as well as other epilepsy indications, include adult focal onset seizures (FOS).

The voltage-gated sodium channel Na_v1.1 is identified as an essential component of the proprioceptive transmission machinery that is required in vivo for normal motor behavior.

Skin-associated bacteria underlie the production of a potent defensive neurotoxin in newts, impacting host physiology, molecular evolution, and predator-prey interactions in a coevolutionary arms race.

Unveiling Na_V1.6's role in sensitizing Slack to quinidine disruption redefines KCNT1-related epilepsy treatment strategies.

Vasoactive intestinal peptide-expressing GABAergic interneurons in cerebral cortex express the sodium channel subunit Nav1.1, and a defined subset of VIP interneurons are dysfunctional in a mouse model of Dravet syndrome.

Neurons mature slower in humans than in other non-human primates.

Expression of a Dravet syndrome-associated mutation in inhibitory neurons disrupts activity of brainstem respiratory neurons and diminishes respiratory behavior in conjunction with seizures and premature death.

Electrophysiology, optogenetics, and imaging in a mouse model of Dravet syndrome reveals dentate gyrus circuit dysfunction driven by hyperexcitability of the perforant path input from entorhinal cortex that can be modulated by recruitment of parvalbumin-expressing inhibitory interneurons.