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Detailed knowledge of cellular expression of G protein-coupled receptors in the human enteric nervous system is essential for understanding their diverse actions.

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      Abstract

      G protein-coupled receptors (GPCRs) comprise a large and diverse superfamily of transmembrane receptors that mediate the functions of an extraordinarily large number of extracellular ligands. They control many major physiological processes and are involved in diverse pathological processes, including gastrointestinal diseases. G protein-coupled receptors are one of the most targeted classes in pharmaceutical drug research. At present, much of our knowledge concerning the expression, distribution and function of GPCRs in the gut has been gleaned from studies performed in experimental models. Data obtained in the human digestive tract, especially in the enteric nervous system, are sparse and incomplete, although enteric neurons have a key position in almost all physiological and pathophysiological processes in the gut. Knowledge of cellular distribution of GPCRs, of regional differences in GPCR expression, and of altered GPCR expression during pathophysiological conditions in the human gut, will lead to a better understanding of GPCR activity, but will also contribute to the development of new drugs. In the current issue of the Journal, Harrington et al. describe the presence and cellular localization of muscarinic receptors in the human colon. Morphologically, orientated studies on the cellular expression of GPCRs in the human gut have to be encouraged, because these studies will yield data that are of therapeutic relevance.

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      Affiliations
      [1 ] Laboratory of Cell Biology & Histology, Department of Veterinary Sciences, University of Antwerp, Antwerpen, Belgium.
      Journal
      Neurogastroenterol. Motil.
      Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
      Wiley
      1365-2982
      1350-1925
      Sep 2010
      : 22
      : 9
      20701687 NMO1575 10.1111/j.1365-2982.2010.01575.x

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