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Anoretic effects of neuropeptide VF are mediated via central mu and kappa subtypes of opioid receptors
Author(s) -
Sliwa Lindsay Nicole,
Cline Mark
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1022.15
Subject(s) - orexigenic , κ opioid receptor , receptor , opioid , medicine , neuropeptide y receptor , endocrinology , antagonist , μ opioid receptor , chemistry , neuropeptide , opioid receptor , receptor antagonist , pharmacology
Recently, we demonstrated that neuropeptide VF (NPVF) causes hypothalamus associated satiety using chicks as models. The present study was designed to better understand some of the central mechanisms that mediate these effects. In experiment 1, co‐injection of NPVF and beta‐funaltrexamine (FNA, a mu opioid receptor antagonist) did not cause a greater suppression of food intake than when NPVF and FNA were injected alone. In experiment 2, co‐injection of NPVF and ICI‐174,864 (ICI, a delta opioid receptor antagonist) caused a more potent reduction in food intake than when NPVF and ICI were injected alone. In experiment 3, co‐injection of NPVF and nor‐binaltorphimine (BNI, a kappa opioid receptor antagonist) did not cause a greater suppression of food intake than when NPVF and BNI were injected alone. The orexigenic effects of neuropeptide Y and beta‐endorphin (both ligands of opioid receptors) were suppressed by NPVF co‐injection. These results suggest that NPVF‐induced satiety has a relationship with mu and kappa but not delta subtypes of opioid receptors, and likely causes suppression of the chick's innate orexigenic system.