Studies on the binding of H-3-dihydroalprenolol (H-3-DHA) to astrocytes from cerebra of normal and hypothyroid rats show that hypothyroidism results in a decline in the beta-adrenergic receptors. Ontogenic studies indicated that in normal, euthyroid rats, the maximum binding capacity (B-max) for H-3-DHA progressively increased with age while the affinity (K-d) remained unaltered. In astrocytes prepared from hypothyroid rats, total number of binding sites for H-3-DHA also increased with age, however, at a given age, the number was significantly lower than that for corresponding euthyroid animals while the affinity for H-3-DHA remained unaffected. Correspondingly, primary cultures of astrocytes from normal and hypothyroid brain when maintained in TH-deficient serum, display 3 similar reduction of H-3-DHA binding. In the case of astrocytes from hypothyroid brain cultured in TH-dfficient serum, the decline can be largely restored by supplementing with normal serum. Results suggest that thyroid hormones (TH) directly or indirectly regulates the level of beta-adrenergic receptors in astrocytes from developing rat brain.