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. 2005 Feb 18:5:5.
doi: 10.1186/1471-230X-5-5.

Central neuropeptide Y receptors are involved in 3rd ventricular ghrelin induced alteration of colonic transit time in conscious fed rats

Johannes J Tebbe  1 , Clemens G Tebbe, Silke Mronga, Michael Ritter, Martin K H Schäfer
Affiliations

Central neuropeptide Y receptors are involved in 3rd ventricular ghrelin induced alteration of colonic transit time in conscious fed rats

Johannes J Tebbe et al. BMC Gastroenterol. .

Abstract

Background: Feeding related peptides have been shown to be additionally involved in the central autonomic control of gastrointestinal functions. Recent studies have shown that ghrelin, a stomach-derived orexigenic peptide, is involved in the autonomic regulation of GI function besides feeding behavior. Pharmacological evidence indicates that ghrelin effects on food intake are mediated by neuropeptide Y in the central nervous system.

Methods: In the present study we examine the role of ghrelin in the central autonomic control of GI motility using intracerobroventricular and IP microinjections in a freely moving conscious rat model. Further the hypothesis that a functional relationship between NPY and ghrelin within the CNS exists was addressed.

Results: ICV injections of ghrelin (0.03 nmol, 0.3 nmol and 3.0 nmol/5 microl and saline controls) decreased the colonic transit time up to 43%. IP injections of ghrelin (0.3 nmol - 3.0 nmol kg(-1) BW and saline controls) decreased colonic transit time dose related. Central administration of the NPY1 receptor antagonist, BIBP-3226, prior to centrally or peripherally administration of ghrelin antagonized the ghrelin induced stimulation of colonic transit. On the contrary ICV-pretreatment with the NPY2 receptor antagonist, BIIE-0246, failed to modulate the ghrelin induced stimulation of colonic motility.

Conclusion: The results suggest that ghrelin acts in the central nervous system to modulate gastrointestinal motor function utilizing NPY1 receptor dependent mechanisms.

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Figures

Figure 1
Figure 1
Effect of ghrelin injected into the 3rd ventricle (ICV) and intraperitoneally (IP) on colonic transit time. Ghrelin injected ICV as well as IP induced a dosed-related stimulation of propulsive colonic motor activity. MI = microinjection The bars represent the mean ± SEM. * P < 0.05 vs. vehicle. ■ = vehicle-group; A = 0.03 nmol ghrelin /5 μl 0.15 M saline; B = 0.3 nmol ghrelin /5 μl 0.15 M saline; C = 3 nmol ghrelin /5 μl 0.15 M saline; D = 0.3 nmol ghrelin kg-1 BW; E = 3.0 nmol ghrelin kg-1 BW
Figure 2
Figure 2
Effect of pretreatment with NPY receptor antagonists on fasted motor activity of the colon induced by centrally (ICV) and peripherally (IP) administered ghrelin. BIBP-3226, which is a selective NPY Y1 receptor antagonist, injected ICV antagonizes the stimulation of colonic transit induced by ghrelin injected in the same route and IP. The NPY Y2 receptor antagonist BIIE-2046 injected ICV fails to affect the stimulated colonic motoractivity induced by ICV or IP injection of ghrelin. MI = microinjection The bars represent the mean ± SEM. * P < 0.05 vs. vehicle-group; #P < 0.05 vs. ghrelin-group
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References

    1. Mönnikes H, Tebbe J, Bauer C, Grote C, Arnold R. Neuropeptide Y in the paraventricular nucleus of the hypothalamus stimulates colonic transit by peripheral cholinergic and central CRF pathways. Neurogastroenterol Moilt. 2000;12:343–352. doi: 10.1046/j.1365-2982.2000.00212.x. - DOI - PubMed
    1. Asakawa A, Inui A, Kaga T, Yuzuriha H, Nagata T, Ueno N, Makino S, Fujimiya M, Niijima A, Fujino MA, Kasuga M. Ghrelin is an appetite-stimulatory signal from stomach with structural resemblance to motilin. Gastroenterology. 2001;120:337–345. - PubMed
    1. Date Y, Kojima M, Hosoda H, Sawaguchi A, Mondal MS, Suganuma T, Matsukura S, Kangawa K, Nakazato M. Ghrelin a novel growth hormone releasing acylated peptide, is synthesized in a distinct endocrine cell type in the gastrointestinal tract of rats and humans. Endocrinology. 2000;141:4255–4261. doi: 10.1210/en.141.11.4255. - DOI - PubMed
    1. Kojima M, Mosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999;402:656–660. doi: 10.1038/45230. - DOI - PubMed
    1. Nakazato M, Murakami N, Date Y, Kojima M, Matsuo H, Kangawa K, Matsukura S. A role for ghrelin in the central regulation of feeding. Nature. 2001;409:194–198. doi: 10.1038/35051587. - DOI - PubMed

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