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Submitted on January 30, 2003
Accepted on May 7, 2003
1 Endocrine Unit, Imperial College London, Hammersmith Campus, Du Cane Rd, London W12 ONN, UK
* To whom correspondence should be addressed. E-mail: s.bloom{at}imperial.ac.uk.
The hypothalamic neuropeptide melanin-concentrating hormone (MCH) increases feeding when injected intracerebroventricularly in rats. To identify the hypothalamic nuclei responsible for the orexigenic effect we injected the peptide into discrete hypothalamic nuclei known to express the MCH receptor, MCH1R. MCH (0.6 nmol) elicited a rapid and significant increase in feeding in satiated rats following injection into the arcuate nucleus (0-1 h: 421 ± 60%; P < 0.01). An elevation in feeding was also observed following injection into the paraventricular nucleus which was sustained up to 4 h post-injection (0-4 h: 218 ± 29%; P < 0.01). A significant increase in feeding during this time period was also observed following injection into the dorsomedial nucleus (0-4 h: 155 ± 12%; P < 0.05). No significant alteration in feeding was observed following injection into the supraoptic nucleus, lateral hypothalamic area, medial preoptic area, anterior hypothalamic area or ventromedial nucleus of the hypothalamus. To identify the neurotransmitters that may be potentially involved in this effect we examined their release from hypothalamic explants in vitro following exogenous MCH administration. MCH (1 µM) increased the release of the orexigenic neurotransmitters neuropeptide Y (37.8 ± 6.0fmol/explant vs. basal 30.2 ± 4.3fmol/explant; P < 0.05) and Agouti related peptide (4.1 ± 0.6fmol/explant vs. basal 2.4 ± 0.2fmol/explant; P < 0.05) and decreased the release of the anorectic neurotransmitters 
-melanocyte stimulating hormone (41.7 ± 6.8fmol/explant vs. basal 65.9 ± 11.0fmol/explant; P < 0.01) and Cocaine- and amphetamine-regulated transcript (112.3 ± 12.4fmol/explant vs. basal 167.4 ± 13.0fmol/explant; P < 0.001). These studies suggest that the orexigenic effect of MCH may be mediated via activation or inhibition of these feeding circuits within the ARC and PVN of the hypothalamus.
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