Polyunsaturated fatty acids facilitate or impede Kv7 channel activation, depending on channel subtype and their dominant functional site(s).

The phytocannabinoid cannabidiol, an antiepileptic agent whose molecular targets are unclear, was found to potently enhance current carried by cloned human Kv7.2/7.3 channels and native M-current in mouse and rat neurons.

Neuronal neurofascin takes a surprisingly circuitous route in the neuronal plasma membrane to the axon initial segment where it stabilises ion channel complexes responsible for initiating action potentials.

In the cochlea, repressor element 1-silencing transcription factor (REST) regulates the expression levels of K_v7.4 and alterations of REST functions result in progressive hearing loss.

Calmodulin mediates in the protective augmentation of K_V7-currents in response to oxidative stress in a calcium-dependent manner by an unconventional signaling mechanism.

Molecular and electrophysiological evidence shows that Kv3 subunits contribute critically to ultrashort action potential waveforms and high-frequency firing in large projection neurons in zebra finch motor nuclei controlling song production and somatic movements.

The structure of a voltage-activated potassium channel in lipid nanodiscs solved using cryo-electron microscopy is similar to previous X-ray structures, and provides insights into the mechanism of C-type inactivation.

In mouse models of Huntington's disease, striatal spiny projection neurons up-regulate dendritic potassium channels, which impairs their normal function, but a zinc finger gene therapy can reverse this deficit.

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.

Analysis of AnkyrinR conditional knockout mice shows that AnkyrinR regulates PV+ fast-spiking interneurons by organizing and maintaining perineuronal nets and through the membrane clustering of Kv3.1b K⁺ channels.