Actions of Thyroid Hormones on Myelination

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.