Morphine, applied by microiontophoresis to functionally identified dorsal horn neurones in segments L5–L7 of cats (chloralose anaesthetized, decerebrated or high spinal), produced primarily a depression of the discharge of neurones responding to noxious radiant heat applied to the skin. It depressed on-going activity (12 out of 20 neurones), glutamate-evoked excitation (8/8) and the response to the noxious stimulus (13/21). The response of two additional neurones to heat was potentiated. The effects began 10–30 s from the onset of application, reached a maximum in up to 8 min and outlasted application by up to 10 min. Morphine had relatively little effect on on-going activity and glutamate-evoked excitation of neurones responding to non-noxious stimuli (n = 18). Naloxone (intravenously and iontophoretic) reversed these depressions (4/11). It is suggested that morphine may produce analgesia, at least in part, by a direct action on a specific morphine receptor in the spinal cord.