Ontogenesis of 3,5,3′-Triiodothyronine Receptors in Neonatal Rat Brain: Dissociation between Receptor Concentration and Stimulation of Oxygen Consumption by 3,5,3′-Triiodothyronine*

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Abstract
The concentration of T3 [3,5,3''-Triiodothyronine] nuclear receptors in the brain of the developing rat was studied. Efforts were made to correlate such concentrations to the level of circulating T3 and to the period during which T3 exerts its maximal effects on maturation of the CNS. The effect of T3 on O2 consumption by slices of neonatal and adult brain was tested in order to determine whether or not neonatal brain, unlike adult brain, is responsive to T3 by this criterion. Receptor sites were demonstrated in fetal whole brain with a binding capacity of 0.17 .+-. 0.02 ng T3/mg DNA, a value only slightly lower than in adult brain (0.22 .+-. 0.03 ng T3mg DNA). Two days after birth, the binding capacity had risen sharply to 0.38 .+-. 0.04 ng T3/mg DNA. During the subsequent 4 wk, the binding capacity fell to adult levels. Plasma T3 concentrations were exceedingly low in the fetal serum (0.08 .+-. 0.01 ng/ml) despite the near normal nuclear binding capacity of brain. A rapid increase in plama T3 was noted from the day after birth (0.04 .+-. 0.01 ng/ml) to the 11th day when the plasma T3 concentration was well within the normal range (0.60 .+-. 0.09 ng/ml). The period of rapid increase in plasma T3 concentration seems to correspond to that period during which T3 exerts its most decisive maturational effects on the CNS. These results may suggest that T3 effects are mediated by 2 coordinated processes. The 1st of these seems to be independent of circulating T3 and results in a high nuclear receptor concentration by the second day after life. The 2nd process is responsible for the thyroidal secretion of thyroid hormone and the conversion of T4 to T3 by peripheral tissues. Probably neither adult nor neonatal brain slices respond with increased O2 consumption to the administration of T3. Apparently this finding fails to support a previous report which suggested that T3 can stimulate O2 consumption in neonatal brain. Failure of brain tissue to respond to T3 with O2 consumption is not due to a paucity of receptor sites, as the binding capacity in the neonatal brain was only slightly less than that in adult liver, a tissue which responds briskly to T3 administration. Appropriate biochemical parameters for measuring the effects of T3 on brain tissue remain largely undefined.