A cationic molecule derived from an uncharged Cav2.2 calcium channel inhibitor powerfully inhibits both sodium and calcium channels with extracellular application and inhibits both pain and neurogenic inflammation.
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.
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 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 ion channel accessory subunit KChIP2 has a transcriptional role that provides regulation over miRNA targets, driving the adverse remodeling of key ion channels during cardiac stress and leading to the development of arrhythmia.