MYELINATION

Myelination is the process by which axons are insulated with a myelin sheath, a lipid-rich membrane that increases the speed of nerve impulse conduction and supports axonal health. In the central nervous system (CNS), oligodendrocytes extend processes that wrap around axons to form segments of compact myelin called internodes, separated by gaps known as nodes of Ranvier. In the peripheral nervous system (PNS), Schwann cells perform a similar function, myelinating a single axon segment each.

Myelin is highly lipid-dense and contains specific proteins that stabilize the sheath. In the CNS, major proteins include myelin basic protein (MBP) and proteolipid protein (PLP); in the PNS, myelin protein zero (P0) is a primary structural component. The insulating layers reduce membrane capacitance and increase electrical resistance, enabling saltatory conduction where action potentials jump between nodes of Ranvier. Conduction velocity depends on axon diameter and the degree of myelination; the g-ratio, the ratio of the inner axon diameter to the total fiber diameter, is typically around 0.6–0.7.

Development and plasticity: myelination begins prenatally in some tracts and continues into young adulthood in many brain regions. Oligodendrocyte precursor cells differentiate into myelinating oligodendrocytes, and activity-dependent signals can influence the timing and extent of myelination.

Clinical relevance: demyelinating diseases disrupt conduction, notably multiple sclerosis in the CNS and Guillain-Barré syndrome in the PNS. Remyelination can occur, with varying efficiency; in the CNS it is primarily by oligodendrocytes, while in the PNS it is mediated by Schwann cells. Myelination also provides metabolic support to axons, contributing to long-term axonal integrity.