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P. A. McGrath, J. R. Bourke, G. J. Huxham and S. W. Manley

ABSTRACT

The membrane potential of cultured porcine thyroid follicular cells depolarized by up to 20 mV from the resting value of about − 73 mV on exposure to β-adrenoceptor agonists. A similar response was induced by TSH or dibutyryl cyclic AMP. α-Adrenoceptor agonists were without effect. The receptor subtype was shown to be (at least predominantly) β2 by the order of potency for β-agonists (isoprenaline ≅ fenoterol⪢adrenaline >noradrenaline) and by the relative potency of selective β-antagonists (ICI 118,551 ⪢atenolol). The α-agonist phenylephrine had no effect on the TSH response but weakly inhibited the β-agonist response. Rather than a physiological antagonism between α- and β-adrenoceptor-mediated responses, this effect was shown to be due to the weak β-antagonist effect of phenylephrine since the α-antagonist phentolamine failed to potentiate the depolarizing response to the mixed agonist nor-adrenaline, and also failed to block the inhibitory action of phenylephrine on the β-agonist effect. Sensitivity to β-agonist was enhanced by omission of serum from the culture medium and reduced by exposure to β-agonists or a high concentration of TSH or dibutyryl cyclic AMP.

J. Endocr. (1985) 107, 23–30

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P. A. McGrath, J. R. Bourke, G. J. Huxham and S. W. Manley

ABSTRACT

Cultured porcine thyroid cells, maintained in the differentiated state by dibutyryl cyclic AMP, responded to serotonin (5-HT; 10 nmol/l to 1 μmol/l) with a depolarization of the membrane potential, but did not respond to histamine (100 μmol/l) or dopamine (1 μmol/l). The resting membrane potential of these cells was about − 71 mV, maximal concentrations of 5-HT (1 μmol/l) inducing a depolarization to approximately −53 mV. Methysergide or phenoxybenzamine, but not propranolol, abolished the response to 5-HT. Sensitivity to 5-HT was reduced by previous exposure of cultures to TSH, the β-adrenoceptor agonist salbutamol or 5-HT itself.

J. Endocr. (1985) 107, 397–401

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J. R. Bourke, P. A. McGrath, G. J. Huxham, M. J. Waters and S. W. Manley

ABSTRACT

Cultured porcine thyroid cells maintained in media containing TSH exhibited a membrane potential of −50 mV, and hyperpolarized by about 10 mV within 1 h of the addition of epidermal growth factor (EGF; 10 ng/ml). Follicle cells had depolarized to −45 mV after 4 h of exposure to EGF. Cells maintained in dibutyryl cyclic AMP (dbcAMP) did not alter their membrane potential when exposed to EGF for up to 4 h. Cultures washed to remove the TSH or dbcAMP hyperpolarized to − 75 mV within 30 min, and a reversible depolarization to − 60 mV was observed on addition of EGF. It was concluded that EGF acts as a physiological antagonist of TSH and also exerts a separate depolarizing influence on cultured thyroid cells.

J. Endocr. (1986) 109, 321–324