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).

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.

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.

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

Variants in FGF13, associated with developmental and epileptic encephalopathies, alter neuronal excitability by affecting inhibitory neurons and by a sodium channel-independent mechanism.

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.

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.

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