Studies on the binding of 3H-dihydroalprenolol (3H-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 (Bmax) for 3H-DHA progressively increased with age while the affinity (Kd) remained unaltered. In astrocytes prepared from hypothyroid rats, total number of binding sites for 3H-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 3H-DHA remained unaffected. Correspondingly, primary cultures of astrocytes from normal and hypothyroid brain when maintained in TH-deficient serum, display a similar reduction of 3H-DHA binding. In the case of astrocytes from hypothyroid brain cultured in TH-deficient 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.