Hyperpolarization of thyroid cells in vitro by thyrotropin and cyclic AMP

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Abstract
With the use of microelectrodes, membrane potential (MP) was measured in mouse thyroid glands in vitro. A basal resting MP of about -39 mV was confirmed. The initial effect of feeding a low-iodine diet (6-12 days) was hyperpolarization up to -47 mV; chronic low-iodine diet led to depolarization. Low concentrations of thyrotropin (< 3 milliunits[mU]/ml superfusate) caused hyperpolarization and high ones (> 10 mU/ml) led to depolarization. Cyclic(c)AMP (10-3 M), dibutyryl cAMP (1.2 .times. 10-4 M or 1.2 .times. 10-3 M) and theophylline (10-2 or 10-3 M) caused similar hyperpolarization; D- and DL-propranolol (5 .times. 10-5-5 .times. 10-4 M) produced depolarization and inhibited hyperpolarization by thyrotropin. Conclusions are that hyperpolarization is a consequence of short-term increased secretion of thyrotropin in vivo or of low (near physiological) concentrations in vitro; these effects are probably mediated by cAMP. The relationship to and mechanism of depolarization resulting from chronic enhanced endogenous secretion or high in vitro concentrations of thyrotropin are unknown.