The PRMT1 protein mediates arginine methylation of KCNQ2 channels to control neuronal excitability.

Mice that successfully avoid developing tinnitus despite exposure to excessive noise show spontaneous recovery of KCNQ2/3 potassium channel activity associated with a reduction in HCN channel activity in auditory brainstem neurons.

Because voltage-gated KCNQ2 channels are central to physiological and pathophysiological events, understanding how disease-causing mutations in different channel regions disrupt function will help future development of mutation-specific antiepileptic therapies.

Contrary to a generally accepted principle, the pore properties of KCNQ1 channels depend on the states of voltage-sensing domains activation; KCNE1 alters the voltage-sensing domains-pore coupling to modulate KCNQ1 channel properties.

ML277 exclusively enhances the AO state voltage-sensing domain (VSD)-pore coupling of KCNQ1 channels, providing an effective tool to investigate the voltge-dependent gating and new strategies for treating long QT syndrome.

Glutamatergic neurons lacking the mitochondrial pyruvate carrier show reduced M-type potassium channel activity and hyperexcitability upon intense firing.

Fatty acid analogues are interesting prototype compounds that may inspire the development of future I_Ks channel activators to treat patients with long QT syndrome caused by diverse arrhythmia-causing mutations in the I_Ks channel.

Aging reduces the potassium M current in sympathetic motor neurons, resulting in a hyperactive phenotype that can be reversed by pharmacological activation of these channels.

A single amino acid change in a neuronal ion channel called KCNQ2 blocks ion flow, prevents protein localization on axons, and results in severe epilepsy and slowed neurological development.

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.