Abstract
The control of myelination in the central nervous system is a classical action
of thyroid hormones. In rodents, thyroid hormone deficiency during the fetal and
postnatal periods delays central myelin deposition and oligodendrocyte gene
expression. Oligodendrocytes differentiate from precursor cells (OPC), originating
from radial glial cells in the ventricular and subventricular zones after multiple cell fate
decisions controlled by developmental genes. The interplay between growth factors
acting at the cell membranes and nuclear receptors, such as those for T3 and retinoic
acid, regulates OPC differentiation. Growth factors promote OPC proliferation, and the
liganded nuclear receptors promote cell cycle exit. Myelination occurs in axons that
reach a critical size, and thyroid hormone might also indirectly affect myelination
through axonal maturation effects. In the clinical setting, myelination can be analyzed
by magnetic resonance imaging in hypothyroid states with variable results.
Keywords: Axons, Allan-Herndon-Dudley syndrome, Cell cycle, Congenital hypothyroidism, Myelin, MBP, Magnetic resonance, Nuclear receptors, OPC, Oligodendrocytes, PDGF, PLP, OLIG2, SHH, White matter.
