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Mechanisms of neuropeptide AF‐induced anorexia in chickens
Author(s) -
Newmyer Brandon,
Siegel Paul,
Cline Mark
Publication year - 2010
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.24.1_supplement.994.5
Subject(s) - anorexia , medicine , endocrinology , anorectic , receptor , neuropeptide , food intake , opioid , κ opioid receptor , neuropeptide y receptor , psychology
Recently we demonstrated an anorectic effect of neuropeptide AF (NPAF). The present study was designed to further elucidate mechanisms mediating NPAF‐induced anorexia and to test in hypo‐ and hyperphagia animals. In Exp 1–3, blockade of the mu and kappa but not delta subtypes of opioid receptors and co‐injection of NPAF did not have an additive anorexic effect, suggesting NPAF is associated with mu and kappa opioid receptors. In Exp 4–5, NPAF injection into both divisions of the paraventricular nucleus (PVN) did not affect food or water intake. In Exp 6, NPAF was centrally injected and food intake was quantified in lines of chicks that have undergone long‐term divergent selection for low (LWS) or high (HWS) body weight and are models of hypo‐ and hyperphagic respectively. LWS chicks responded 120 min sooner and their threshold was 4 orders lower than noted in HWS chicks. In Exp 7, several behaviors were quantified, and feeding and exploratory pecks, time spent standing and sitting were all reduced, but not differentially between lines. However, total distance moved was reduced in LWS‐ but not HWS‐NPAF‐treated chicks. Also, LWS‐ slept more while HWS‐NPAF‐treated chicks slept less. These data support that NPAF‐induced anorexia is mediated through opioid receptors, that the PVN is not primary activated in NPAF‐induced anorexia, and hypo‐ and hyperphagic individuals respond differently to NPAF.