The action of the thyroid hormones in the adipose tissue, the liver, the heart, the muscles and the bones are expressed during neonatal but not fetal life. It is not known whether this delay in the action of the thyroid hormones in these tissues is related to the maturation of the thyroid hormone signaling pathway at a molecular level or related to the maturation of thyroid hormone metabolism. The actions of the thyroid hormones, which are specific to each individual tissue, depend on the prevalent isoform of the thyroid hormone receptor (TR) which is expressed in each tissue and on cofactors at the site of action of the thyroid hormones. The highest concentrations of TRs are found in developing neurons and in various regions in the brain of the fetus and the neonate such as cortex, cerebellum, and visual and auditory cortices. There are many indications that the TR^1 isoform of the receptor is the one which promotes, via T3, the vital development of the central nervous system in the fetus, the neonate and the child in combination with the a1 receptor [39, 40]. It is of interest that the deafness that exists in the TRp 1 knockout rat also exists in endemic cretinism in some patients with resistance to thyroid hormones due to lack of the TR^1 gene .
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