Intracellular recordings were made from neurons of the rat locus coeruleus in a slice of tissue cut from the pons and superfused in vitro at 37 degrees C. Both acetylcholine, in the presence of a muscarinic antagonist, and nicotine depolarized locus coeruleus neurons and increased the rate of action potential discharge. These effects persisted in a superfusing solution that contained no calcium ions and a raised magnesium ion concentration; because such solutions block synaptic potentials in the locus coeruleus, it was concluded that the acetylcholine and nicotine acted directly on the cell from which the recording was made. Acetylcholine-evoked depolarizations were blocked by hexamethonium or dihydro-beta-erythroidine, but not by alpha-bungarotoxin. Recordings of membrane current showed that acetylcholine and nicotine caused a net inward current, the amplitude of which increased linearly as the membrane potential was changed from -40 to -90 mV; the extrapolated reversal potential was about -20 mV (extracellular potassium concentration was 2.5 mmol/l). Depolarizations caused by nicotine declined during the presence of the agonist when the period of superfusion was continued for more than 2 min; repeated applications of nicotine evoked reproducible depolarizations only when the interval between them was at least 1 h. It is concluded that neurons of the rat locus coeruleus have nicotinic receptors with properties similar to those in peripheral ganglia with respect to reversal potential for the ion channel, insensitivity to alpha-bungarotoxin and propensity to desensitize.