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.
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.
Directly targeting the ribosome to attenuate translation partly mimics the integrated stress response, increasing lifespan and preserving protein folding capacity even in older individuals with dysfunctional stress response signaling.
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.
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.