Anoretic effects of neuropeptide FF are mediated via central mu and kappa subtypes of opioid receptors and receptor ligands.

Mark A Cline, Derrick S Mathews

Index: Gen. Comp. Endocrinol. 159(2-3) , 125-9, (2008)

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Abstract

Recently, we demonstrated that neuropeptide FF (NPFF) causes anorexigenic effects in chicks that were associated with the hypothalamus. The present study was designed to better understand some of the central mechanisms that mediate these effects. Co-injection of NPFF and beta-funaltrexamine (FNA, a mu opioid receptor antagonist) did not suppress food intake more than when NPFF and FNA were injected alone. However, co-injection of NPFF and ICI-174,864 (ICI, a delta opioid receptor antagonist) caused a greater reduction in food intake than when NPFF and ICI were injected alone. Co-injection of NPFF and nor-binaltorphimine (BNI, a kappa opioid receptor antagonist) did not cause a greater suppression of food intake than when NPFF and BNI were injected alone. Hyperphagia induced by neuropeptide Y and beta-endorphin (both ligands of opioid receptors) was reversed by NPFF. These results suggest that NPFF-induced satiety has a relationship with mu and kappa but not delta subtypes of opioid receptors, and since NPFF does not bind opioid receptors itself NPFF-associated satiety is likely mediated by effects on opioid receptor ligands such as NPY and beta-endorphin. Thus, NPFF induced satiety may be mediated via modulation of the chick's innate opioid-associated orexigenic system.