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.

Regulation of Cav2.3 Ca²⁺ channels by membrane-bound β2 subunit splice variants permits long-lasting channel activity even during prolonged and continuous activity in dopamine neurons, with implications for Parkinson's disease pathophysiology.

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.

The feedback inhibition of T-type calcium channels by intracellular calcium provides new avenues to better decipher the roles of these low-voltage-activated channels in the fine control of calcium signaling events in physiology and pathophysiology.

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.

The Caenorhabditis elegans presynapse contains two pools of synaptic vesicles at the active zone, coupled to either neuronal-type or muscle-type calcium channels, and to different docking machinery.

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).

Human sensory neurons may not only bridge a critical gap between drug discovery and clinical trials, but force a re-evaluation of basic assumptions about the mechanisms controlling primary afferent excitability.

The direct interaction of R-type Ca²⁺ channel Cav2.3 and GABA_B receptor auxiliary subunits in the active zone of medial habenula terminals scales synaptic strength independent of GABA_B receptor activation.

Specific deletion of Cav3.2 channels in anterior pretectal neurons reduced mechanical and cold allodynia, pointing to Cav3.2 channels as prime targets to develop innovative analgesic pharmacology that will not only act at the peripheral level but also in central structures.