ZDHHC14 controls palmitoylation and axon initial segment targeting of PSD93 and Kv1-family potassium channels, events that are essential for normal neuronal excitability.

The voltage-sensing mechanism of a subfamily of potassium channels is modulated in unconventional ways by an amino acid transporter.

Type 1 potassium channels alter their composition and localisation to suppress hyper-excitability and neuropathic pain of injured sensory neurons.

The structure of KvAP addresses a mechanism of voltage-dependent gating that has been debated for 16 years.

Dysfunctions of myelin peroxisomes cause a lysosomal storage-like disorder associated with alterations in glial and axonal membranes, which is the likely cause of nerve impairment in peroxisomal disorders.

A-type potassium conductances influence the distinctive firing behaviour of irregular-spiking interneurons.

The mechanosensitive potassium channel TRAAK is localized to nodes of Ranvier is mammalian axons where it hyperpolarizes the resting potential and may contribute to mechanical repolarization of neurons.

Dysmyelination of GABAergic hippocampal interneurons causes mislocalization of axonal ionic channels and disturbs their intrinsic physiological properties, suggesting that it may contribute to cognitive deficits observed in multiple sclerosis patients.

Analysis of iconic and gating currents of wild type and mutated BK channels reveals a strong inhibition of this channel by extracellular acidification and elucidates the underlying mechanism that is potentially applicable to other voltage-dependent cation channels.