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Melanocortin receptor activation regulates the release of NPY from rat hypothalamus in vitro
Author(s) -
Murphy Beth Ann,
Jochnowitz Nina,
Strack Alison,
Martin William
Publication year - 2006
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.20.5.a830-c
Subject(s) - neuropeptide y receptor , melanocortin , medicine , endocrinology , hypothalamus , melanocortins , melanocortin receptor , melanocortin 4 receptor , agonist , receptor , chemistry , stimulation , receptor antagonist , neuropeptide , antagonist , biology
A function of the hypothalamus is to integrate energy‐related signals. Two peptide systems within this region that regulate responses to changes in caloric state are Neuropeptide Y (NPY) and melanocortins (MC). NPY and MC stimulate and suppress food intake, respectively. The purposes of this study were 1) to evaluate the effect of food restriction on electrically‐induced NPY release from isolated rat hypothalamus, and; 2) to determine if synthetic MC receptor agonists and antagonists could alter the release of NPY. Isolated rat hypothalami were incubated in a superfusion system and stimulated electrically (50mA, 25 Hz, 2.5 min) in the absence and presence of MCR agonist/antagonists. NPY content of superfusates were analyzed by RIA. Electrical stimulation caused NPY to increase 10‐fold in food restricted rats, but only 1.5‐fold in rats with free access to food. Application of the MCR antagonist SHU9119 enhanced electrically‐stimulated NPY release compared to levels from untreated tissue. Co‐application of THIQ, an MC4R specific agonist, partially blocked the SHU9119 effect. These results confirm that feeding state influences hypothalamic NPY release. Furthermore, the degree of MCR activation alters the extent of NPY release and the MC4R subtype contributes to this process. These results suggest that monitoring NPY release may be useful for understanding the receptor systems that modulate energy balance.