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The paraventricular nucleus of the hypothalamus is a neuroanatomical substrate for the inhibition of palatable food intake by neuropeptide S
Author(s) -
Fedeli Amalia,
Braconi Simone,
Economidou Daina,
Cannella Nazzareno,
Kallupi Marsida,
Guerrini Remo,
Calò Girolamo,
Cifani Carlo,
Massi Maurizio,
Ciccocioppo Roberto
Publication year - 2009
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2009.06948.x
Subject(s) - medicine , endocrinology , anorectic , hypothalamus , chemistry , antagonist , nucleus accumbens , neuropeptide , anxiolytic , receptor , neuropeptide y receptor , lateral hypothalamus , food intake , biology
Neuropeptide S (NPS) is a recently discovered neurotransmitter that binds to its cognate G‐protein coupled receptor, NPSR. Previous studies have shown that central administration of this peptide induces anxiolytic‐like effects, promotes arousal and inhibits feeding in the same dose range. In the present study, we sought to investigate further the unique physiopharmacological profile of the NPS system by characterizing its effects on palatable food consumption in rats and comparing it with the effect of the classical anxiolytic benzodiazepine midazolam. The results demonstrated that midazolam (5.0 or 10.0 mg/kg) increases palatable food consumption, while intracerebroventricular (ICV) administration of NPS markedly reduces it. The anorectic effect of NPS (0.1–1.0 nmol per rat, ICV) was prevented by ICV pretreatment with the NPSR antagonist [ d ‐Cys(tBU) 5 ]NPS (20.0–60.0 nmol per rat). Pretreatment with the nonselective corticotrophin‐releasing factor receptor (CRF) antagonist alpha‐helical CRF 9–41 (6.25 and 12.5 nmol per rat) completely reversed the hypophagic action of CRF (0.4 nmol per rat, ICV) but did not prevent the anorectic effect of ICV NPS (1.0 nmol per rat). Brain site‐specific microinjection experiments revealed that NPS markedly inhibits palatable food intake if administered into the paraventricular nucleus of the hypothalamus (PVN). A similar but smaller and shorter lasting reduction of feeding was observed following intra‐lateral hypothalamus administration, whereas no effect was observed following injection into the central amygdala. The present study demonstrates that NPS evokes a potent inhibition of palatable food consumption and that the PVN is an important site of action for its effect.