Abstract:
:Neuropeptide VF (NPVF) induces satiety through hypothalamic interactions; however, the central mechanism that mediates these effects is poorly understood. Therefore, this study was conducted to explore some possible opioid receptor associated mechanisms of NPVF-induced satiety using chicks as models. Co-injection of NPVF and a mu opioid receptor antagonist (beta-funaltrexamine, FNA) did not have an additive suppressive effect on food intake compared to NPVF and FNA when injected alone. Contrary, co-injection of NPVF and a delta opioid receptor antagonist (ICI-174,864, ICI) caused a greater reduction in food intake than when both were injected alone. Co-injection of NPVF and a kappa opioid receptor antagonist (nor-binaltorphimine, BNI) did not cause an additive suppressive effect on food intake than when the two were injected alone. A reversal of neuropeptide Y and beta-endorphin induction of food intake occurred when NPVF was co-injected. These results support that NPVF-induced satiety is mediated through mu and kappa but not delta subtypes of opioid receptors, and their ligands including neuropeptide Y and beta-endorphin. Thus, NPVF-associated anorexia may be mediated via modulation of the chick's innate opioid-associated orexigenic system.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Cline MA,Sliwa LNdoi
10.1016/j.neulet.2009.03.029subject
Has Abstractpub_date
2009-05-22 00:00:00pages
195-8issue
3eissn
0304-3940issn
1872-7972pii
S0304-3940(09)00324-3journal_volume
455pub_type
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