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

doi:10.1186/1471-230X-5-5

BMC Gastroenterology

Volume 5

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Tebbe JJ
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Mronga S
Ritter M
Schäfer MK

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Schäfer MK
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Research article

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

Johannes J Tebbe¹ , Clemens G Tebbe¹ , Silke Mronga¹ , Michael Ritter² and Martin KH Schäfer³

¹Department of Internal Medicine, Division Gastroenterology – Endocrinology, Philipps Universität Marburg, 35033 Marburg, Germany

²Department of Internal Medicine, Division Cardiology, Philipps Universität Marburg, 35033 Marburg, Germany

³Department of Molecular Neuroscience, Institute of Anatomy and Cell Biology, Philipps Universität Marburg, 35033 Marburg, Germany

author email corresponding author email

BMC Gastroenterology 2005, 5:5doi:10.1186/1471-230X-5-5


Published:	18 February 2005

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 μl and saline controls) decreased the colonic transit time up to 43%. IP injections of ghrelin (0.3 nmol – 3.0 nmol kg^-1BW and saline controls) decreased colonic transit time dose related. Central administration of the NPY₁receptor 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 NPY₂receptor 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 NPY₁receptor dependent mechanisms.