Many laboratories have reported that systemically administered naloxone has little or no effect on lateral hypothalamic self-stimulation (LH In the present study, lateral ventricular infusion of β-endorphin antiserum and a high dose of naloxone (100μg) produced small but significant increases in stimulation frequency threshold for LH ICSS. β-Endorphin activity, mediated by a non-μ (e.g. δ or ɛ) receptor, may therefore be involved in the reinforcement of self-stimulation behavior. When rats are deprived of food for 24 h, LH ICSS thresholds decline. Under this condition, systemic naloxone elevates the LH ICSS threshold, often returning it to the pre-deprivation level. In the present study, lateral ventricular infusion of dynorphin A(1–13) antiserum similarly reversed the threshold-lowering effect of food deprivation. The effects of systemic naloxone and intraventricular dynorphin A antiserum on LH ICSS, which are specific to food-deprived animals, may be related to previous findings that these two treatments elevate LH stimulation threshold for eliciting feeding behavior. Results of the ICSS and stimulation-induced feeding studies suggest a model for the mediation of incentive stimuli by dynorphin A activity that is afferent to LH ‘reward’ neurons and positively gated by ‘hunger’. An hypothesized role for ‘hunger’-gated dynorphin A release in potentiating the hedonic response to alimentary stimuli and drugs of abuse is discussed.