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The non-opiate beta-endorphin fragment des-Tyr1-gamma-endorphin (DT gamma E) had a decreasing effect on K+-induced release of tritiated dopamine from nucleus accumbens slices in vitro, when tissue was used of rats which prior to decapitation were in a state of low arousal. When nucleus accumbens tissue was used of rats which were mildly stressed by exposure to a novel environment prior to decapitation, this effect was absent, while an enhancing effect of DT gamma E became evident on basal dopamine efflux. This latter effect resembled that of haloperidol, which dose-dependently enhanced basal dopamine efflux in vitro. Exposure of rats to ether vapor shortly before decapitation abolished both these in vitro effects of DT gamma E. The results are interpreted as indicating that the quality of the modulating effects of DT gamma E on dopamine release from dopaminergic neurons projecting to the nucleus accumbens is depending on the state of activity of these neurons, which, in its turn, is a reflection of the state of arousal of the rats.