Thyroid control maturation

Complex biological processes often require coordinated control of the expression of many genes. The maturation of a tadpole into a frog is largely controlled by thyroid hormone. This hormone regulates gene expression by binding to a protein, the thyroid hormone receptor, shown at the left. 

The thyroid hormones control metabolism. They increase cardiac output and the excitability of the nervous system. In children, the maturing of the cerebral cortex, of the skeleton, the musculature and the genitalia, is stimulated. Both hormones are active only in their protein-imbound state. Free thyroxine and 3,3 ,5-triiodothyronine bind to receptors in the ceU nucleus and in the mitochondria, where they activate protein synthesis and the production of adenosine triphosphate. 

Microtubule ausserobly from hypothyroid preparations (Fig.2) was also tested (19,20) at day 15 postnatal the polymerization activity was similar to that measured at earlier stages O-S days) with the euthyroid preparations. Analysis of the MAPs present at day 15 postnatad also showed a hi ier proportion of immature Tau than in the control of the same age (20). Hiis suggested that the transition betsi een juvenile and mature Tau is delayed in hypothyroidism, a conclusion i ch mi it be sufficient to e3q)lain the lower polymerization activity produced by thyroid hormone deficiency. 

There are a number of possibilities that could account for the interaction between thyroid hormone and NGF. For example, treatments with insulin and insulin-like growth factor II have been found to increase specific and saturable NGF binding sites in cultured human neuroblastoma cells.It is possible that analogous mechanisms between thyroid hormone and NGF may operate in subcortical cholinergic cells. Another possibility could be that if thyroid hormone controls the formation of ChAT or of proteins essential for cholinergic cell maturation at a pretranslational level S and NGF regulates the de novo synthesis of these crucial proteins at transcriptional level,30 then a combination of these effects could synergistically potentiate ChAT activity. 

Histologic study shows that the histologic features of the thyroid gland of the iodine treated fetuses were comparable to normal control fetuses. In the 4th - 5th month fetuses, the thyroid gland showed distinct formation of follicles lined with small cuboidal epithelial cells and containing scanty colloid. In the 6th - 8th month fetuses, the thyroid tissue showed more mature differentiation. The follicle size and the amount and staining density of the colloid increased with the fetal age. 

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