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Wrap membrane around axons to form myelin insulation in CNS. Enable saltatory conduction. Myelin is compacted, insulating membrane with little cytoplasm. Disruption causes demyelinating disorders.
From your study of saltatory conduction, you know that myelin sheaths wrap around axons and force action potentials to jump between nodes of Ranvier, dramatically increasing conduction speed. In the central nervous system, the cells responsible for producing this myelin are oligodendrocytes — a class of glial cells whose name literally means "cells with few branches," though those few branches do remarkable work.
A single oligodendrocyte extends several flat, sheet-like processes, each of which wraps concentrically around a segment of a nearby axon. Imagine wrapping a strip of tape around a wire — each turn adds another layer of insulation. The oligodendrocyte's membrane is extraordinarily rich in lipid (about 70% by dry weight), particularly myelin basic protein (MBP) and proteolipid protein (PLP), which help compact the membrane layers tightly together with very little cytoplasm between them. This compaction is critical: the tightly packed lipid bilayers create a high-resistance, low-capacitance sheath that prevents ion leakage across the axon membrane, which is exactly what makes saltatory conduction possible.
One key difference from the peripheral nervous system is worth noting. In the PNS, Schwann cells perform myelination, but each Schwann cell wraps only a single axon segment. An oligodendrocyte, by contrast, can myelinate segments on up to 40–50 different axons simultaneously. This efficiency comes at a cost: if a single oligodendrocyte is damaged or dies, dozens of axon segments lose their myelin at once. This is exactly what happens in multiple sclerosis (MS), where the immune system attacks oligodendrocytes and their myelin. The resulting demyelinated patches — called plaques — slow or block signal conduction along the affected axons, producing symptoms that depend on which tracts are involved: vision problems when optic nerve myelin is damaged, weakness when motor tracts are affected, numbness when sensory pathways lose insulation.
Oligodendrocytes are also metabolically coupled to the axons they myelinate. They supply lactate and other metabolites to the underlying axon through channels in the myelin sheath, meaning the relationship is not merely insulation but active metabolic support. This explains why demyelination does not just slow signals — it can eventually lead to axonal degeneration if the metabolic support is withdrawn for too long. Understanding oligodendrocyte biology is therefore central to developing therapies for demyelinating diseases, and current research focuses on promoting remyelination by stimulating oligodendrocyte precursor cells that persist in the adult brain.