Production of remyelinating subventricular zone oligodendrocyte progenitors is stimulated by transient abrogation of thyroid hormone signalling in the adult neural stem cell niche.

Electrically active axons in white matter stimulate their own myelination by releasing glutamate, which signals through AMPA-type glutamate receptors on nearby oligodendrocyte precursors and newly-differentiating oligodendrocytes, enhancing their survival and hence their ability to myelinate.

Endogenous synthesis of fatty acids by oligodendrocytes is essential for development and repair in the central nervous system.

Oligodendrocytes in white matter use Kir4.1 inwardly rectifying potassium channels to prevent extracellular potassium accumulation, enabling neurons to sustain repetitive firing and limiting the initiation of seizures.

In oligodendrocyte progenitor cells, lipid metabolism and peroxisome biogenesis are regulated by the low-density lipoprotein related-receptor-1, and if disrupted, impair proper white matter development and adult repair.

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

Ultrastructural and loss-of-function experiments show that oligodendrocyte-encoded Kir4.1 is located near active axonal structures, including within myelin inner tongue, and has critical functions to promote axonal activity and preserve integrity.

The signaling lipid PI(3,5)P₂ supports the formation of the myelin sheath, by regulating trafficking of myelin building blocks within oligodendrocytes and communication between oligodendrocytes and neuronal axons.

Oligodendrocytes are actively engaged in the precise control of synaptic functions in the CNS through activity-dependent BDNF signaling.

A combined approach of unbiased proteomics, biochemistry, genetics, and transgenic animal models reveals that GPR56/ADGRG1 regulates myelin formation and repair by interacting with its microglial-derived ligand transglutaminase 2.