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.
Polyunsaturated fatty acid analogues show selectivity for different cardiac ion channels, suggesting their potential use for the treatment of different subtypes of Long QT Syndrome.
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.
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.
A human cellular model of a prototypical form of intractable childhood epilepsy supports selective impairment of inhibitory neurons as a key pathophysiological mechanism.
CaV1.3 channels of the short isoform are coupled via their C-terminal domains in a Ca2+-CaM-dependent manner, which facilitates Ca2+ influx and increases the discharge of hippocampal neurons.
Computer simulations show that the firing patterns of branched touch receptors can be set in part by the organization of their sensory endings in the skin.
