Abstract: | Chronic food restriction produces a variety of physiological and behavioral adaptations including a potentiation of the reinforcing effect of food, drugs and lateral hypothalamic electrical stimulation. Previous work in this laboratory has revealed that the lowering of self-stimulation threshold by food restriction is reduced by μ- and κ-selective opioid antagonists. In the present study, the effect of chronic food restriction on levels of three prodynorphin-derived peptides, namely dynorphin A1–17 (A1–17), dynorphin A1–8 (A1–8) and dynorphin B1–13 (B1–13) were measured in eleven brain regions known to be involved in appetite, taste and reward. Food restriction increased levels of A1–17 in dorsal medial (+ 19.6%), ventral medial (+ 24.2%) and medial preoptic (+ 82.9%) hypothalamic areas. Levels of A1–17 decreased in the central nucleus of the amygdala (− 35.1%). Food restriction increased levels of A1–8 in nucleus accumbens (+ 34.4%), bed nucleus of the stria terminalis (+ 24.5%) and lateral hypothalamus (+ 41.9%). Food restriction had no effect on levels of B1–13. A1–17 is highly κ-preferring and the brain regions in which levels increased all have a high ratio of κ:μ and δ receptors. A1–8 is less discriminating among opioid receptor types and the brain regions in which levels increased have a low ratio of κ:μ and δ receptors. The present results suggest that food restriction alters posttranslational processing within the dynorphin A domain of the prodynorphin precursor, possibly leading to a change in the balance between κ and non-κ opioid receptor stimulation in specific brain regions. |