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Extracellular recordings were made from spontaneously active arcuate neurones in hypothalamic slices in vitro. The majority of these neurones (82%) were inhibited in a dose-related manner by opioid peptides added to the perfusion medium at concentrations of 0.1-100 microM. The inhibitory responses were reversed by equimolar concentrations of naloxone. In terms of their latency to 50% inhibition and duration of action the order of potency of the opioid peptides on a molar basis was beta-Endorphin greater than DAGO greater than DADLE greater than Dynorphin. Several sub-populations of arcuate neurones can be identified on the basis of their neuronal activity. Opioid peptides selectively abolished the bursts in those neurones (putative peptidergic neurones) which discharged with a combination of bursts and single irregular action potentials suggesting a selective membrane action rather than an overall hyperpolarizing influence. A population of neurones which displayed episodic or regular activity, and which had action potentials characteristic of dopamine neurones, were profoundly inhibited by the opioid peptides; the activity of a second population of regularly firing neurones with conventional action potential profiles was totally unaffected. These electrophysiological studies thus provide evidence that the arcuate nucleus is one possible site of action at which endogenous opioid peptides could exert their modulatory role on neuroendocrine function; and the predominate influence is likely to be mediated through mu receptors.