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1 Department of Medicine, Division Hepatology and Gastroenterology, Charite, Campus Virchow-Klinikum, Freie Universitat and Humboldt-Universitat Berlin, Berlin, Germany
2 Department of Medicine, Division Gastroenterology and Endocrinology, Philipps-Universitat Marburg, Marburg, Germany
3 Robert-Koch-Institute, Berlin, Germany
4 Department of Medicine, Division Psychosomatic Medicine and Psychotherapy, Charite, Campus Charite Mitte, Freie Universitat and Humboldt-Universitat Berlin, Berlin, Germany
5 Institute of Anatomy, Section of Electron, Microscopy and Neuroanatomy, Charite, Campus Charite Mitte, Freie Universitat and Humboldt-Universitat Berlin, Berlin, Germany
6 Department of Medicine, CURE Digestive Diseases Research Center, Center for Neurosvisceral Sciences, Digestive Diseases Divison UCLA and VA Greater Los Angeles Healthcare System, Los Angeles, CA, USA
7 Department of Medicine, Division Hepatology and Gastroenterology, Charite, Campus Virchow-Klinikum, Freie Universitat and Humboldt-Universitat Berlin, Berlin, Germany; Department of Medicine, Division Psychosomatic Medicine and Psychotherapy, Charite, Campus Charite Mitte, Freie Universitat and Humboldt-Universitat Berlin, Berlin, Germany
* To whom correspondence should be addressed. E-mail: hubert.moennikes{at}charite.de.
Cholecystokinin (CCK) and ghrelin exert antagonistic effects on ingestive behavior. The aim of the present study was to investigate the interaction between ghrelin and CCK administered peripherally on food intake and neuronal activity in specific hypothalamic and brainstem nuclei, as assessed by c-Fos-like immunoreactivity (c-FLI) in non fasted rats. Ghrelin (13 µg/kg-BW) injected intraperitoneally (ip) significantly increased the cumulative food intake when measured at 30 min and 1 h after injection compared to the vehicle group (2.9 ±1.0 g/kg-BW vs. 1.2 ± 0.5 g/kg-BW, p<0.028). CCK-8S (2 or 25 µg/kg-BW) injected simultaneously blocked the orexigenic effect of ghrelin (0.22 ± 0.13 g/kg-BW, p<0.001 and 0.33 ± 0.23 g/kg-BW, p<0.0008) while injected alone, both doses of CCK-8S exerted a non significant trend to reduce food intake. Ghrelin (13 µg/kg-BW,ip) markedly increased the number of c-FLI positive neurons/section in the arcuate nucleus (ARC) compared to vehicle (median: 31.35 vs. 9.86, p<0.0001). CCK-8S (2 or 25 µg /kg-BW ip)had no effect on neuronal activity in the ARC, as assessed by c-FLI (median: 5.33 and 11.21 cells/section) but blocked the ghrelin-induced increase of c-fos expression in this area when both peptides were administered simultaneously (median: 13.33 and 12.86 cells/section, respectively). Ghrelin at this dose had no effect on CCK-induced stimulatation of c-fos expression in the paraventricular nucleus of the hypothalamus (PVN) and the nucleus of the solitary tract (NTS). These results suggest that CCK abolishes ghrelin-induced food intake through dampening increased ARC neuronal activity.
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