Alpha 2- and beta-adrenergic receptors and adenosine A1 receptor of FRTL-5 rat thyroid cells in relation to fucosyl GM1 ganglioside.

We have previously reported that anti-fucosyl GM1 ganglioside antibody partially suppresses cAMP production in FRTL-5 rat thyroid cells not via the TSH receptor but via guanine nucleotide-binding protein indirectly. In order to clarify further the mechanism of the antibody action, we studied the relationship with alpha 2- and beta-adrenergic and adenosine A1 receptors. FRTL-5 cells did not bind [3H]clonidine, suggesting the lack of alpha 2-adrenergic receptor or at least abnormality of its binding domain. On the other hand, the cells specifically bound [125I]iodocyanopindolol, but isoproterenol failed to affect the basal and TSH-stimulated cAMP production indicating the lack of coupling with adenylate cyclase. The inhibition of cAMP production induced by anti-fucosyl GM1 antibody was not altered by adrenergic agents. [125I]hydroxyphenylisopropyl adenosine binding was observed in FRTL-5 cells but was not displaced by the antibody. These results lead to conclusions that FRTL-5 cells lack alpha 2-adrenergic receptor but have beta-adrenergic receptor which lacks coupling with adenylate cyclase and have adenosine A1 receptor, and that the adrenergic receptors and adenosine A1 receptor are not the site of action of anti-fucosyl GM1 antibody.