Oligonucleotide probes complementary to specific regions of three thyroid receptor cDNAs were used to study the effects of thyroid hormone on the expression of the mRNAs encoding two alpha (alpha 1 and alpha 2) and one beta-thyroid (beta 1) receptors isoforms in rat cerebral hemisphere astrocyte cultures. Both genes are expressed by type 1 astrocytes. The levels of the alpha 1-, alpha 2-, and beta 1-mRNAs did not significantly change between day 8 and day 22, in cultures grown in the absence of thyroid hormone. L-triiodothyronine (L-T3) treatment of the cultures increased the levels of beta 1-mRNAs by fivefold without changing either the levels of the alpha 1- and alpha 2-mRNAs or L-T3 binding capacity. The effect of L-T3 on beta 1-mRNAs was observed after 4 h of treatment and was independent of protein synthesis, suggesting that this effect is likely to be a direct one. Treatment of the cultures by cytosine arabinosine, a drug that kills dividing cells, specifically decreased level of the alpha 1- and alpha 2-mRNAs by 60% and 38%, respectively. Finally, by immunocytochemistry, we showed that the beta 1 receptor-immunoreactivity was either located in the perinuclear region and the cytoplasm or in the nuclei of astrocytes. Taken together with previous data obtained in neuronal cultures where no effect of L-T3 was observed on the levels of the beta 1-mRNAs, our findings indicate that the beta 1 gene is differentially regulated in neurons and astrocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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