Experimental and modeling results reveal that the activation of resurgent sodium currents relies on the recovery of inactivated channels into a conducting state, and that the decay of resurgent currents reflects the accumulation of these channels into a slow-inactivated state.

An epilepsy-associated potassium channel variant causes neuron-type-dependent alterations in ionic currents, neuronal excitability, and network connectivity.

The phytocannabinoid cannabidiol, an antiepileptic agent whose molecular targets are unclear, was found to potently enhance current carried by cloned human Kv7.2/7.3 channels and native M-current in mouse and rat neurons.

Transient weakness in myotonia congenita is caused by depolarization secondary to activation of persistent Na⁺ current in skeletal muscle.

In cortical pyramidal neurons, subtype-specific SUMOylation of Na+ channels regulates input-output relationships, synaptic boosting, and action potential propagation from the axonal trigger zone back into the dendrites.

A-type fibroblast growth factor homologous factors generate resurgent currents in tetrodotoxin-resistant voltage-gated sodium channels, increase repetitive firing of sensory neurons, and provide a potentially important target for pain treatment strategies.

Calpain is a promising therapeutic target to reduce spasticity after a spinal cord injury.

Computational modeling motivated by recent experiments clarifies biophysical mechanisms generating the rhythm and amplitude of breathing at the level of neurons and brain circuits in mammals.

A simple mechanism, based on the synergy of two major opposing voltage-dependent currents that are ubiquitous in neurons, produces functional diversity of developing Renshaw cells in the embryo.

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).