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

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.

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.

Biologically plausible levels of myelin dystrophy induce substantial working memory impairment in a computational model of brain aging across two spatial and temporal scales.

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.

Single and double-knockout mouse models for proteins associated with nodes of Ranvier reveal that a paranodal, spectrin-based lateral diffusion barrier is sufficient to cluster Na+ channels at nodes of Ranvier.

Glial TDP-43 regulates splicing and expression of neurofascin and is required for proper assembly and maintenance of paranodal axoglial junctions.

Oligodendrocyte precursor cells receive brain-wide, circuit-specific intracortical, coritcocortical and thalamocortical synaptic inputs.

Node of Ranvier length is similar at successive nodes along single myelinated CNS axons, but differs between axons, and could potentially be tuned to adjust the conduction velocity of each axon.