PRL-releasing peptide inhibit food intake in male rats via the dorsomedialhypothalamic nucleus and not the paraventricular hypothalamic nucleus

PRL-releasing peptide inhibits food intake after intracerebroventricular in jection. PRL-releasing peptide immunoreactivity is found in several hypotha lamic nuclei involved in feeding, with highest levels in the paraventricula r and dorsomedial hypothalamic nuclei. The aim of this study was to examine tt effect of PRL-releasing peptide on food intake after administration int o these nuclei. Paraventricular nucleus injection of PRL-releasing peptide did not alter fo od intake. Dorsomedial hypothalamic nucleus injection of PRL-releasing pept ide decreased 1 h food intake [PRL-releasing peptide (1 nmol) 83.4 +/- 6.1% saline all; P < 0.05]; and continued until 8 h postinjection. [PRL-releasi ng peptide (1 nmol) 89.2 +/- 4.1% saline; P < 0.05]. To investigate the mechanism of this inhibition of food intake, we examined PRL-releasing peptide's effect on neuropeptide release from hypothalamic e xplants. alpha MSH release was increased [PRL-releasing peptide (100 mnol), 5.4 +/- 1.6 pmol/explant; change vs. basal, P < 0.01], whereas agoutirelat ed protein release was unchanged. The release of cocaine-and amphetamine-re gulated transcript was inhibited [PRL-releasing peptide (100 nmol), -33.5. +/- 12.6 pmol/explant; change vs. basal, P < 0.01]. PRL-releasing peptide d ose-dependently increased neurotensin release [PRL-releasing peptide (1 nmo l), 3.7 +/- 2.6 pmol/explant; change vs. basal, P = NS; PRL-releasing pepti de (10 nmol), 7.2 +/- 2.7 pmol/explant; change vs. basal, P < 0.01; PRL-rel easing peptide (100 nmol), 36.8 +/- 5.4 pmol/explant; change vs. basal, P < 0.001]. Our data suggest that the dorsomedial hypothalamic nucleus is important in the inhibitory effect of PRL-releasing peptide on food intake and that PRL- releasing peptide alters the release of several hypothalamic neuropeptides important in the control of food intake.