Electrophysiological and pharmacological properties of cultured rat thyroid cells.

The electrophysiological properties of a hormone-dependent, differentiated thyroid epithelial cell strain were studied using intracellular microelectrodes. The average membrane potential of solitary, isolated cells was -78.4 +/- 1.3 mV. The membrane potential depolarized 55 mV per tenfold increase in extracellular potassium concentration. Weak electrical coupling was recorded between contiguous cells. Like thyroid cells in vivo, these cells did not generate action potentials. In some cells a spontaneous, slow transition in the membrane potential from -80mV to -30 mV was accompanied by an increase in input resistance. Membrane potential transitions could be induced by perfusing cells with isotonic Hanks solutions saturated with CO2 (pH = 5.5) or by perfusing cells with hypotonic Hanks solutions (190-290 mOsm/kg). Membrane potential transitions were due to a decreased potassium permeability. Noradrenaline elicited both a fast depolarization and a slow depolarization. The fast depolarization was due to an increase in conductance of Na+ channels and of Cl- channels. Intracellular injection of Ca++ elicited the fast depolarization. Intracellular injection of EGTA or cobalt abolished the fast depolarization. Replacement of extracellular Ca++ by Mg++ did not affect the fast depolarization. Thus, the fast depolarization was due to accumulation of intracellular Ca++. The fast depolarization was abolished by the alpha adrenergic blocker phentolamine (10(-6) M), and was not abolished by the beta adrenergic blocker propranolol (10(-5) M).