Decrease in beta-adrenergic receptors of cerebral astrocytes in hypothyroid rat brain.
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.
Das
S
S
Cell Biology Division, Indian Institute of Chemical Biology, Calcutta.
Paul
S
S
D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000648:ultrastructure*; D001921:Brain / Q000254:growth & development / Q000378:metabolism / Q000648:ultrastructure*; D002478:Cells, Cultured; D004082:Dihydroalprenolol / Q000378:metabolism; D005260:Female; D007037:Hypothyroidism / Q000378:metabolism*; D007700:Kinetics; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D014316:Tritium
D011943:Receptors, Adrenergic, beta; D014316:Tritium; D004082:Dihydroalprenolol