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Acta Physiologica Congress

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Acta Physiologica 2009; Volume 196, Supplement 671
Scandinavian Physiological Society’s Annual Meeting
8/14/2009-8/16/2009
Uppsala, Sweden


ROLE OF ENTERIC NETWORK BEHAVIOUR IN DIARRHOEAL DISEASE
Abstract number: L12

Sjovall1 H

1Institue to Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. [email protected]

The enteric nervous system operates largely independently of the central nervous system. It processes very large amounts of sensory information (mechanosensory and chemosensory) resulting in motor, secretomotor and vasomotor effector output. This complex system has an inherent propensity to generate a few "default" motor patterns, the two most important ones being the migrating motor complex (MMC) that is activated in the fasting state, and the fed pattern activated after meals. The exact mechanism behind the MMC, a cyclic distally migrating motor and secretory rhythm, is unknown. Myenteric sensory AH neurons are interconnected in recurrent networks enabling positive feedback. Using computer modeling, it has been shown that such networks under certain conditions may go into full synchronized firing that will propagate slowly in the distal direction, i.e. a pattern very similar to phase III of the MMC. During this period, one also sees activation of secretion with a pattern well compatible with network behaviour. It has recently been shown that the secretory component of this system is frequently upregulated in celiac disease, in bile acid malabsorption (BAM) and in diarrhoea-dominated irritable bowel syndrome (IBS). On the basis of pharmacological experiments in anaesthetized rats, using distension as stimulus, the neural mechanisms behind the secretomotor response have been analyzed. The response has several components with involvement of tachykinin receptors, nicotinic receptors and VIP receptors. On the basis of these data, we will tentatively discuss possible mechanisms behind the disturbed MMC-associated secretomotor pattern in celiac disease, BAM and IBS.

To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 196, Supplement 671 :L12

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