Small intestine: Edited by William F. Stenson and David H. AlpersEnteric nervous system: sensory physiology, diarrhea and constipationWood, Jackie D Author Information Department of Physiology and Cell Biology and Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, Ohio, USA Correspondence to Jackie D. Wood, MSc, PhD, AGAF, 304 Hamilton Hall, 1645 Neil Avenue, Columbus, OH 43210-1218, USA Tel: +1 614 292 5449; fax: +1 614 292 4888; e-mail: [email protected] Current Opinion in Gastroenterology: March 2010 - Volume 26 - Issue 2 - p 102-108 doi: 10.1097/MOG.0b013e328334df4f Buy Metrics Abstract Purpose of review The enteric nervous system integrates secretion and motility into homeostatic patterns of behavior susceptible to disorder. Progress in understanding mechanosensory detection in these processes, disordered enteric nervous system integration in diarrhea and constipation and pharmacotherapy is summarized. Recent findings Most neurons in the enteric nervous system discharge in response to distortion. Drugs acting directly to open chloride conductance channels in the mucosal epithelium are therapeutic options for constipation. Summary Mechanoreception is required for negative feedback control. At issue is identification of the neurons that fulfil the requirement for mechanoreception. Understanding secretomotor neurons is basic to understanding neurogenic secretory diarrhea and constipation and therapeutic strategies. A strategy for treatment of chronic constipation is development of agents that act directly to open Cl− channels, which thereby increases the liquidity of the luminal contents. Lubiprostone, a recently Food and Drug Administration-approved drug, increases intraluminal liquidity by opening Cl− channels. The future for the drug is clouded by controversy over whether its action is directly at one or the other of chloride channel type 2 (ClC-2) or cystic fibrosis transmembrane conductance regulator (CFTR) chloride channels or both and whether action reflects involvement of G protein-coupled prostaglandin receptors expressed by mucosal epithelial cells. © 2010 Lippincott Williams & Wilkins, Inc.