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This Article Full Text Full Text (PDF) All Versions of this Article: 290/3/R625    most recent 00639.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Sartor, D. M. Articles by Verberne, A. J. M. Search for Related Content PubMed PubMed Citation Articles by Sartor, D. M. Articles by Verberne, A. J. M.

APPETITE, OBESITY, DIGESTION, AND METABOLISM

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

¹Clinical Pharmacology and Therapeutics Unit, Department of Medicine, and ²Department of Surgery, University of Melbourne, Austin Health, Heidelberg Victoria, Australia

Submitted 31 August 2005 ; accepted in final form 19 October 2005

Ingestion of a meal results in gastrointestinal (GI) hyperemia and is associated with systemic and paracrine release of a number of peptide hormones, including cholecystokinin (CCK) and 5-hydroxytryptamine (5-HT). Systemic administration of CCK octapeptide inhibits a subset of presympathetic neurons of the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor tone to the GI viscera. The aim of this study was to determine whether endogenous release of CCK and/or 5-HT also inhibits CCK-sensitive RVLM neurons. The effects of intraduodenal administration of the secretagogues sodium oleate (SO) and soybean trypsin inhibitor (SBTI) on circulating levels of CCK and 5-HT were examined. In separate experiments, the discharge rates of barosensitive, medullospinal, CCK-sensitive RVLM presympathetic vasomotor neurons were recorded after rapid intraduodenal infusion of SO-SBTI or water. Alternatively, animals were pretreated with the CCK₁ receptor antagonists devazepide and lorglumide or the 5-HT₃ antagonist MDL-72222 before SO-SBTI administration. Secretagogue infusion significantly increased the level of circulating CCK, but not 5-HT. SO-SBTI significantly decreased (58%) the neuronal firing rate of CCK-sensitive RVLM neurons compared with water (5%). CCK₁ receptor antagonists did not reverse SO-SBTI-induced neuronal inhibition (58%), whereas the 5-HT₃ antagonist significantly attenuated the effect (22%). This study demonstrates a functional relation between a subset of RVLM presympathetic vasomotor neurons and meal-related signals arising from the GI tract. It is likely that endogenously released 5-HT acts in a paracrine fashion on GI 5-HT₃ receptors to initiate reflex inhibition of these neurons, resulting in GI vasodilatation by withdrawal of sympathetic tone.

rostroventrolateral medulla; cholecystokinin; devazepide; MDL-72222; 5-hydroxytryptamine

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				S. C. Mobley, D. A. Mandel, and A. M. Schreihofer Systemic Cholecystokinin Differentially Affects Baro-activated GABAergic Neurons in Rat Caudal Ventrolateral Medulla J Neurophysiol, November 1, 2006; 96(5): 2760 - 2768. [Abstract] [Full Text] [PDF]

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