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Effects of cholera toxin on the potential difference and motor responses induced by distension in the rat proximal small intestine in vivo

Journal article
Authors Shirin Kordasti
Maria Sapnara
Evan A. Thomas
Erik Lindstrom
Mikael Forsman
Joel C. Bornstein
Henrik Sjövall
Published in American Journal of Physiology - Gastrointestinal and Liver Physiology
Volume 290
Issue 5
Pages G948-G958
ISSN 0193-1857
Publication year 2006
Published at Institute of Neuroscience and Physiology
Institute of Neuroscience and Physiology, Department of Physiology
Institute of Medicine, Department of Internal Medicine
Pages G948-G958
Language en
Keywords guinea-pig ileum, transmembrane conductance regulator, escherichia-coli enterotoxins, fluid secretion, submucous plexus, myenteric plexus, cystic-fibrosis, distal colon, postsynaptic potentials, gastrointestinal-tract
Subject categories Physiology, Gastroenterology and Hepatology


Cholera toxin (CT) may induce uncontrolled firing in recurrent networks of secretomotor neurons in the submucous plexus. This hypothesis was tested in chloralose-anesthetized rats in vivo. The secretory reflex response to graded intestinal distension was measured with or without prior exposure to luminal CT. The transmural potential difference (PD) was used as a marker for electrogenic chloride secretion. In controls, distension increased PD, and this response was reduced by the neural blocker tetrodotoxin given serosally and the vasoactive intestinal peptide (VIP) receptor antagonist [4Cl-D-Phe(6),Leu(17)]VIP (2 mu g.min(-1).kg(-1) iv) but unaffected by the serotonin 5-HT3 receptor antagonist granisetron, by the nicotinic receptor antagonist hexamethonium, by the muscarinic receptor antagonist atropine, or by the cyclooxygenase inhibitor indomethacin. Basal PD increased significantly with time in CT-exposed segments, an effect blocked by granisetron, by indomethacin, and by [4Cl-D-Phe(6),Leu(17)]VIP but not by hexamethonium or atropine. In contrast, once the increased basal PD produced by CT was established, [4Cl-DPhe(6),Leu(17)] VIP and indomethacin had no significant effect, whereas granisetron and hexamethonium markedly depressed basal PD. CT significantly reduced the increase in PD produced by distension, an effect reversed by granisetron, indomethacin, and atropine. CT also activated a specific motility response to distension, repeated cluster contractions, but only in animals pretreated with granisetron, indomethacin, or atropine. These data are compatible with the hypothesis that CT induces uncontrolled activity in submucous secretory networks. Development of this state depends on 5-HT3 receptors, VIP receptors, and prostaglandin synthesis, whereas its maintenance depends on 5-HT3 and nicotinic receptors but not VIP receptors. The motility effects of CT (probably reflecting myenteric activity) are partially suppressed via a mechanism involving 5-HT3 and muscarinic receptors and prostaglandin synthesis.

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