Enkephalin and opiate analgesic drugs exert their effects on the brain by interacting with receptors located on neuronal membranes. An almost immediate consequence of this interaction is an inhibition of action potential discharge of individual nerve cells1. This could result from a direct hyperpolarization of the neurone which bears the opiate receptors, thereby shifting its membrane away from the threshold for action potential generation. On the other hand, it is well known that opiates and enkephalin depress the release of neurotransmitters2,3, and this could indirectly result in an inhibition of cell firing. Here we describe experiments which indicate that Met5-enkephalin and a stable analogue, D-Ala2-D-Leu5-enkephalin (DADLE), as well as narcotic analgesics, increase the potassium conductance of neurones in the rat locus coeruleus and thereby inhibit then-spontaneous firing. This effect of the opioids results from an interaction with a receptor having a high affinity for naloxone.