A patch-clamp study was conducted on cultured frog pituitary melanotrophs, in order to investigate the effects of adrenaline on the electrical activity of these cells. In the whole-cell configuration, adrenaline (1 µM) caused hyperpolarization that was accompanied by a fall in membrane input resistance and a blockage of spontaneous action potentials. Under voltage clamp, adrenaline elicited a net-outward current. The hyperpolarization became undetectable at a command voltage of –100 mV which corresponded to the equilibrium potential of potassium ions. The effect of adrenaline on membrane potential and spontaneous activity was blocked by the α2-adrenergic receptor antagonist yohimbine (1-10 µM) but could not be mimicked by the α2-adrenergic agonist clonidine (1–10 µM). In the cell-attached configuration, exposure of the extra-patch membrane to adrenaline increased the occurrence of single-channel currents with a slope conductance of 100 pS. The deduced reversal potential of these currents corresponded to the equilibrium potential of potassium ions. These results suggest that frog melanotrophs display an α2-adrenergic receptor subtype coupled to potassium channels involved in hyperpol