The appearance of NG2⁺ glial cells in the dorsal telencephalon of the embryo coincides with the establishment of the brain blood vessel network in mice.

NG2 glial cells respond to synaptic input with calcium signals in the absence of action potentials and process synaptic depolarizations with somatic and dendritic voltage gated channels.

Neuronal Ia-2 and glial Kon coordinate an injury-response insulin relay that restores glial cell populations and induces neural stem cells from glia, enabling central nervous system regeneration.

The discovery of markers specific to perisynaptic Schwann cells will accelerate the discovery of mechanisms important for their differentiation and function.

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.

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.

Neural tube-associated boundary caps are heterogeneous with a non-neural crest-derived subpopulation that may originate from the developing meninges, which gives rise to derivatives that migrate along nerves to detach and differentiate into skin mural cells.

Pericytes surrounding capillaries in the retina contain α-smooth muscle actin, demonstrating that pericytes have the necessary molecular machinery to change capillary diameter during neurovascular coupling.

Loss of the RNA-binding protein TDP-43 impairs the survival of oligodendrocyte progenitors and reactivates growth of mature oligodendrocytes, resulting in inappropriate wrapping of neuronal somata and blood vessels.

Repressing astroglial PTBP1 by shRNA or antisense oligonucleotide fails to convert astrocyte to neuron including dopaminergic neuron in a 6-OHDA mouse model of PD.