They give rise to oligodendrocytes, which then wrap around axons and provide electrical insulation by forming a myelin sheath.
This enables faster action potential propagation and high fidelity transmission without a need for an increase in axonal diameter.
[3] In addition, OPCs express receptors for various neurotransmitters and undergo membrane depolarization when they receive synaptic inputs from neurons.
[4] They are smaller than neurons, of comparable size to other glia, and can either have a bipolar or complex multipolar morphology with processes reaching up to ~50 μm.
[26][27] As development progresses, second and third waves of OPCs originate from Gsh2-expressing cells in the lateral and caudal ganglionic eminences and generate the majority of adult oligodendrocytes.
[22] After the committed progenitor cells exit the germinal zones, they migrate and proliferate locally to eventually occupy the entire CNS parenchyma.
[33] Typically beginning in postnatal development, OPCs myelinate the entire central nervous system (CNS).
Up to 30% of the oligodendrocytes that exist in the adult corpus callosum are generated de novo from OPCs over a period of 2 months.
[42][43] Using NG2-Cre mice, it was shown that OPCs in the prenatal and perinatal grey matter of the ventral forebrain and spinal cord generate protoplasmic type II astrocytes in addition to oligodendrocytes.
[47] In conclusion, these studies suggest that OPCs do not generate a significant number of neurons under normal conditions, and that they are distinct from neural stem cells that reside in the subventricular zone.
[6][54] Under conditions in the developing and mature CNS where a reduction in the normal number of oligodendrocytes or myelin occurs, OPCs react promptly by undergoing increased proliferation.
Rodent OPCs proliferate in response to demyelination in acute or chronic lesions created by chemical agents such as lysolecithin, and newborn cells differentiate into remyelinating oligodendrocytes.
In chronic MS lesions where remyelination is incomplete, there is evidence that there are oligodendrocytes with processes extending toward demyelinated axons, but they do not seem to be able to generate new myelin.
[11][69] Electron microscopy revealed OPC membranes apposed to neuronal presynaptic terminals filled with synaptic vesicles.
However, OPCs appear to lose their ability to respond to synaptic inputs from neurons as they differentiate into mature oligodendrocytes.
OPCs have been increasingly recognized for their pivotal role in modulating immune responses, particularly in autoimmune diseases such as multiple sclerosis.
[73] They are highly responsive to injury, undergo a morphological activation similar to that of astrocytes and microglia, and may contribute to glial scar formation.
Should adult cells be used for transplantation, a brain biopsy would be required for each patient, adding to the risk of immune rejection.
Embryonically derived stem cells have been demonstrated to carry out remyelination under laboratory conditions, but some religious groups are opposed to their use.
[citation needed] Adult central nervous system stem cells have also been shown to generate myelinating oligodendrocytes, but are not readily accessible.
[citation needed] It had been known since the early 1900s that astrocytes, oligodendrocytes, and microglia make up the major glial cell populations in the mammalian CNS.
The presence of another glial cell population had escaped recognition because of the lack of a suitable marker to identify them in tissue sections.
The notion that there exists a population of glial progenitor cells in the developing and mature CNS began to be entertained in the late 1980s by several independent groups.
[85] In a separate series of studies, cells from perinatal rat optic nerves that expressed the A2B5 ganglioside were shown to differentiate into oligodendrocytes in culture.