Intracellular recordings were made from locus coeruleus neurones in slices cut from rat pons and superfused in vitro. Membrane currents were recorded with a single-electrode switch-clamp amplifier. Opioids, enkephalin analogues or morphine, caused a concentration-dependent potassium current, which had a maximum value of about 300 pA at -60 mV. The opioid-sensitive potassium conductance was independent of membrane potential between -60 and -130 mV, but became less as the membrane potential was changed from -60 to -30 mV. The opioid outward current was reduced by quinine (100 microM-1 mM) and barium (30 microM-2 mM), but not by 4-aminopyridine (100 microM-1 mM) or tetraethylammonium (10 mM). A potassium current with similar properties flowed for several seconds after a burst of action potentials; this appeared to result from calcium entering the neurone during the action potentials. The alpha 2-adrenoceptor agonists noradrenaline and clonidine caused a concentration-dependent potassium conductance increase which had the same maximum value as that caused by opioids in the same neurones. Experiments in which an opioid and an alpha 2-adrenoceptor agonist were superfused together indicated that the same potassium conductance is increased by both agonists.