Abstract
Myelin sheaths speed up impulse propagation along the axons of neurons without the need for increasing axon diameter. Subsequently, myelin (which is made by oligodendrocytes in the central nervous system) allows for highly complex yet compact circuitry. Cognitive processes such as learning require central nervous system plasticity throughout life, and much research has focused on the role of neuronal, in particular synaptic, plasticity as a means of altering circuit function. An increasing body of evidence suggests that myelin may also play a role in circuit plasticity and that myelin may be an adaptable structure which could be altered to regulate experience and learning. However, the precise dynamics of myelination throughout life remain unclear – does the production of new myelin require the differentiation of new oligodendrocytes, and/or can existing myelin be remodelled dynamically over time? Here we review recent evidence for both de novo myelination and myelin remodelling from pioneering longitudinal studies of myelin dynamics in vivo, and discuss what remains to be done in order to fully understand how dynamic regulation of myelin affects lifelong circuit function.
Highlights
The human brain undergoes extensive maturation throughout life to facilitate cognitive development
Given the energy cost of such a process, is this mechanism sustainable throughout life in an organ the size of the human brain? Perhaps in the human brain there is limited oligodendrocyte overproduction, because of a need for more protracted myelination of the larger central nervous system (CNS), or because signals such as neuronal activity stimulate oligodendrocyte precursor cells (OPCs) to differentiate into oligodendrocytes as and when required
The CNS is traditionally described by appearance after formaldehyde fixation, where “white matter” describes the heavily myelinated axonal tracts, while “grey matter” describes regions densely packed with neuronal cell bodies, dendrites, and synapses
Summary
The human brain undergoes extensive maturation throughout life to facilitate cognitive development. The myelination of axons throughout the nervous system is one such crucial maturation process. In the central nervous system (CNS), glial cells called oligodendrocytes extend many processes into their surrounding environment, which concentrically wrap membrane around axons to form myelin sheaths. Axons that are fully myelinated along their length conduct impulses many times faster than unmyelinated axons of the same cross sectional size (Waxman, 1980). Myelinated neural circuits conduct information much faster than unmyelinated circuits. Humans are born with a virtually unmyelinated CNS, and the oligodendrocyte population expands dramatically following birth with widespread myelination in the first few years of childhood. The maturation of white matter (the myelin-rich areas of the CNS) is concurrent with development of childhood cognitive processes, such as information processing speed (Mabbott et al, 2006; Scantlebury et al, 2014). Myelin pathology/abnormalities are seen in the demyelinating disease Multiple Sclerosis, and in several neurodegenerative diseases (Kang et al, 2013; Huang et al, 2015) and neurodevelopmental disorders (Takahashi et al, 2011)
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