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.
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.
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.
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.
In the peripheral nervous system, the large GTPase dynamin 2 is required for Schwann cell survival, developmental radial sorting of axons, myelination, and myelin maintenance.
During the second postnatal week, a temporary circuit made up of specific types of neurons plus the precursors of oligodendrocytes is established in the brain, and may promote the maturation of oligodendrocytes in preparation for myelination.
OPC-specific genetic inhibition of Akt upstream and downstream molecules in the mouse, and simultaneous OPC fate analysis reveal that PTEN-AKT-GSK3b forms a persistent negative signaling pathway for OL development, in parallel with the AKT-mTORC1 pathway.
