Abstract
In rat pups, thyroid hormone dependent brain development coincides with the appearance of the thyroid hormone receptor (TR) β1 isoform. This finding led to the suggestion that TR β1 plays an essential role in brain development. The recent availability of a mouse TR β knockout strain allowed us to test this possibility by determining whether TR β is essential for the normal developmental pattern of expression of two thyroid hormone regulated brain genes, myelin basic protein (MBP), and Purkinje cell protein 2 (Pcp-2). Northern analysis of total mRNA from the brains of wild-type mice established that, as in the rat pup, the initial rate of rise of the MBP and Pcp-2 mRNA is slowed in the hypothyroid state. Supporting the effectiveness of TR β gene deletion was the finding that the thiiodothyronine (T3) nuclear binding capacity in the livers and brains of knockout animals was consistent with the fractional contribution of TR β1 to total binding capacity in the wild-type tissues. Further, no TR β1 could be detected by isoform-specific immunoprecipitation of nuclear receptor extracts. However, deletion of the functional TR β in the TR β knockout mice did not affect the normal ontogeny of expression of the Pcp-2 and MBP genes in the postnatal pup. We conclude that TR β is not essential for the normal developmental expression of these T3 dependent brain genes.
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