A teaching module on cellular control of small intestinal motility

Department of Human Physiology and Centre for Neuroscience, Flinders University, Bedford Park, South Australia.
Neurogastroenterology and Motility (Impact Factor: 3.59). 11/2005; 17 Suppl 3(s3):4-19. DOI: 10.1111/j.1365-2982.2005.00712.x
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Available from: Marcello Costa, Oct 07, 2014
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    • "The stomach generates myogenic activity in which electrical slow waves generate rings of contraction that spread from the corpus towards the pyloric sphincter (Hirst & Edwards, 2006). Slow waves generated by interstitial cells of Cajal (ICC) conduct into smooth muscle cells and depolarize the membrane, causing a transient contraction due to mechanically productive Ca 2+ entry via voltage-gated (L-type) Ca 2+ channels (Costa et al. 2005). Removal of Ca 2+ from the cytoplasm by the plasma membrane Ca 2+ -ATPase and the sarcoplasmic reticulum (SR) membrane Ca 2+ -ATPase (SERCA) repolarizes the membrane and relaxes the smooth muscle cells (Sanders, 2008). "
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    ABSTRACT: We investigated intracellular Ca(2+) waves, spontaneous transient outward currents (STOCs), and membrane potentials of gastric antrum smooth muscle cells from wild-type and phospholamban-knockout mice. The NO donor sodium nitroprusside (SNP) increased intracellular Ca(2+) wave activity in wild-type antrum smooth muscle cells, but had no effect on the constitutively elevated intracellular Ca(2+) wave activity of phospholamban-knockout cells. STOC activity was also constitutively elevated in phospholamban-knockout antrum smooth muscle cells relative to wild-type cells. SNP or 8-bromo-cGMP increased the STOC activity of wild-type antrum smooth muscle cells, but had no effect on STOC activity of phospholamban-knockout cells. Iberiotoxin, but not apamin, inhibited STOC activity in wild-type and phospholamban-knockout antrum smooth muscle cells. In the presence of SNP, STOC activity in wild-type and phospholamban-knockout antrum smooth muscle cells was inhibited by ryanodine, but not 2-APB. The cGMP-dependent protein kinase inhibitor KT5823 reversed the increase in STOC activity evoked by SNP in wild-type antrum smooth muscle cells, but had no effect on STOC activity in phospholamban-knockout cells. The resting membrane potential of phospholamban-knockout antrum smooth muscle cells was hyperpolarized by approximately -6 mV compared to wild-type cells. SNP hyperpolarized the resting membrane potential of wild-type antrum smooth muscle cells to a greater extent than phospholamban-knockout antrum smooth muscles. Despite the hyperpolarized membrane potential, slow wave activity was significantly increased in phospholamban-knockout antrum smooth muscles compared to wild-type smooth muscles. These results suggest that phospholamban is an important component of the mechanisms regulating the electrical properties of gastric antrum smooth muscles.
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    ABSTRACT: Gastrointestinal (GI) motility and functional GI disorders are common reasons for patients to see gastroenterologists. Knowledge of the evaluation and treatment of these disorders is important to appropriately care for these patients in clinical practice. Training in GI motility is important to GI fellows and their subsequent role as gastroenterologists. The aim of this paper is to discuss the importance of GI motility disorders for trainees in gastroenterology, provide some suggestions for training activities for GI fellows in GI motility, and discuss ways to address the unmet clinical need for caring for patients with GI motility disorders that gastroenterologists routinely see in their clinical practice.
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    ABSTRACT: Sepsis is a systemic inflammatory response representing the leading cause of death in critically ill patients, mostly due to multiple organ failure. The gastrointestinal tract plays a pivotal role in the pathogenesis of sepsis-induced multiple organ failure through intestinal barrier dysfunction, bacterial translocation and ileus. In this review we address the role of the gastrointestinal tract, the mediators, cell types and transduction pathways involved, based on experimental data obtained from models of inflammation-induced ileus and (preliminary) clinical data. The complex interplay within the gastrointestinal wall between mast cells, residential macrophages and glial cells on the one hand, and neurons and smooth muscle cells on the other hand, involves intracellular signaling pathways, Toll-like receptors and a plethora of neuroactive substances such as nitric oxide, prostaglandins, cytokines, chemokines, growth factors, tryptases and hormones. Multidirectional signaling between the different components in the gastrointestinal wall, the spinal cord and central nervous system impacts inflammation and its consequences. We propose that novel therapeutic strategies should target inflammation on the one hand and gastrointestinal motility, gastrointestinal sensitivity and even pain signaling on the other hand, for instance by impeding afferent neuronal signaling, by activation of the vagal anti-inflammatory pathway or by the use of pharmacological agents such as ghrelin and ghrelin agonists or drugs interfering with the endocannabinoid system.
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