Electrical stimulation in lateral hypothalamic sites (ESLH) supporting appetitive behavior and reward also diminishes pain and aversion responses that are organized high in the neuraxis. A paired-pulse stimulation technique was used, in two different behavioral paradigms, to infer the absolute refractory periods of LH neurons that mediate this apparent supraspinal analgesia. In both paradigms, recovery from refractoriness--reflected by increased analgesic action--was evident at intrapair intervals of 0.8 msec and greater. This finding suggests that the overlap, if any, between first stage neurons mediating analgesia and appetitive/reward behavior may be restricted to the 'heterogeneous slow population' distinguished by Gratton and Wise. The dopamine antagonist pimozide, at doses known to diminish ESLH-induced feeding and reward (0.25 and 0.5 mg/kg), failed to affect analgesia. Thus, the dopaminergic second stage neurons deemed critical to feeding and reward may not play an important role in analgesia. Finally, ESLH-induced ameliorative action as a case of 'aversion-gating' or a dimension of classical somatosensory analgesia is discussed.