Description |
1 online resource (162 pages) : illustrations (some color) |
Series |
Integrated systems physiology, from molecule to function to disease ; #26 |
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Colloquium series on integrated systems physiology ; #26.
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Contents |
1. Introduction |
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2. Historical perspective -- 2.1 Neurogastroenterology |
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3. Heuristic model |
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4. Microanatomy -- 4.1 Myenteric plexus -- 4.2 Submucosal plexus -- 4.3 Enteric ganglia -- 4.4 Neuronal morphology |
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5. Sensory neurophysiology -- 5.1 Sensory neurons -- 5.2 Mechanoreception -- 5.3 Intramural sensory detection -- 5.3.1 Low- and high-threshold mechanoreceptors -- 5.4 Visceral pain -- 5.5 Visceral hypersensitivity in the irritable bowel syndrome -- 5.6 Sensory translation in the cerebral cortex -- 5.7 Sensory translation in the spinal cord -- 5.7.1 Central sensitization ("wind-up") -- 5.8 Ascending enteric pain pathways in the spinal cord -- 5.9 Descending spinal pain modulation -- 5.10 Vagal afferents -- 5.11 Chemoreception -- 5.11.1 Cholecystokinin receptors on vagal afferents -- 5.11.2 Serotonergic 5-HT3 receptors on vagal afferents -- 5.11.3 Serotonergic 5-HT3 receptors and the irritable bowel syndrome |
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6. Interneurons |
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7. Enteric motor neurons -- 7.1 Secretomotor and secretomotor/vasodilator neurons -- 7.1.1 Inhibitory synaptic input to secretomotor neurons -- 7.1.2 Secretory diarrhea and constipation -- 7.1.3 Excitatory synaptic input to secretomotor neurons -- 7.2 Excitatory musculomotor neurons -- 7.3 Inhibitory musculomotor neurons -- 7.3.1 Physiological significance of inhibitory musculomotor neurons -- 7.3.2 Ongoing discharge of inhibitory musculomotor neurons -- 7.3.3 Inhibitory musculomotor control of sphincters and intestinal musculature |
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8. Disinhibitory motor disorders -- 8.1. Chronic intestinal pseudoobstruction -- 8.2 Inflammatory enteric neuropathies -- 8.3 Sphincteric achalasia |
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9. Neuronal electrical behavior -- 9.1 AH-type ENS neurons -- 9.1.1 Resting membrane potentials in AH-type neurons -- 9.1.2 Action potentials in AH-type neurons -- 9.2 S-type ENS neurons -- 9.2.1 Action potentials in S-type neurons |
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10. Synaptic transmission -- 10.1 Fast excitatory postsynaptic potentials -- 10.1.1 Nicotinic receptors -- 10.1.2 Purinergic receptors -- 10.1.3 Serotonergic 5-HT3 receptors -- 10.2. Fast EPSP rundown -- 10.3 Fast EPSPs: significance -- 10.4 Slow synaptic, endocrine, and paracrine excitation -- 10.4.1 Slow EPSPs -- 10.4.2 Slow EPSPs in AH neurons -- 10.4.3 Slow EPSPs in S-type neurons -- 10.4.4 Slow EPSP mediators -- 10.4.5 Metabotropic signal transduction -- 10.4.6 Metabotropic transduction in AH-type neurons -- 10.4.7 Adenosine receptors -- 10.4.8 Adenosine 5'-monophosphate -- 10.4.9 Suppression of resting CA2+ influx in AH-type neurons -- 10.4.10 Metabotropic transduction in S-type neurons -- 10.5 Significance of slow EPSPs in the integrated ENS -- 10.6 Inhibitory postsynaptic potentials -- 10.6.1 Ionic mechanisms for slow IPSPs. -- 10.7 Slow IPSP mediators -- 10.7.1 Opiate/opioid receptors -- 10.7.2 Norepinephrine, galanin, somatostatin, serotonin, and purinergic mediators -- 10.8 Significance of slow IPSPs in the integrated system -- 10.9 Presynaptic facilitation -- 10.10 Presynaptic inhibition -- 10.10.1 Mediators of presynaptic inhibition -- 10.10.2 Norepinephrine -- 10.10.3 Significance of sympathetic noradrenergic presynaptic inhibition -- 10.10.4 Immune/inflammatory mediators -- 10.10.5 Serotonin -- 10.10.6 Acetylcholine -- 10.10.7 Pancreatic polypeptide, PYY, and NPY -- 10.10.8 Adenosine -- 10.10.9 Galanin |
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11. Organ level integration |
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12. Gastric motor integration -- 12.1 ENS-brainstem cooperative interactions -- 12.2 Vago-vagal reflexes -- 12.3 Antral pump -- 12.3.1 Neural control of the central pump -- 12.4 Gastric reservoir -- 12.4.1 Gastric reservoir relaxation -- 12.5 Gastric emptying |
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13. Integrated control of the small and large intestines -- 13.1 Intestinal musculature -- 13.2 ENS neural control -- 13.2.1 Intestinal propulsive motility -- 13.2.2 Peristaltic retropulsion -- 13.2.3 Physiological ileus -- 13.2.4 Intestinal power propulsion |
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14. Plasticity in the ENS -- 14.1 Enteric stem cells -- 14.2 Gastric reflex plasticity -- 14.3 Secretomotor plasticity -- 14.4 ENS plasticity in Hirschsprung's disease -- 14.5 Plasticity at the microcircuit level of neural organization -- 14.5.1 Histaminergic neuromodulation -- 14.5.2 Serotonergic neuromodulation -- 14.6 Presynaptic inhibitory modulation -- 14.7 Central pattern generators -- 14.7.1 Histamine-evoked pattern generator |
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15. Small intestine motility -- 15.1 Interdigestive motor program -- 15.1.1 Adaptive significance of the MMC -- 15.2 Digestive motor program -- 15.2.1 Vagal nerve commands -- 15.3 Power propulsion |
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16. Defecation -- 16.1 Recto-anal reflex -- 16.1.1 Stem cell restoration and repair of ENS reflexes -- 16.2 Motility of the large intestine -- 16.3 Pelvic floor musculature -- 16.4 Sensory neurons |
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References -- Author biography |
Summary |
Minute-to-minute behavior of the alimentary tract reflects the integrated functioning of the gut's musculature, secretory glands and blood-lymphatic vasculature. Activity of the three effector systems to generate functionally effective patterns of behavior, which are adaptive for differing digestive states, is organized and coordinated by the enteric nervous system (i.e., the brain-in-the-gut). The heuristic model for the enteric nervous system (ENS) is the same as for all integrative nervous systems, whether in vertebrate or invertebrate animals. Like other integrative nervous systems, such as the spinal cord and brain stem, the ENS functions with sensory neurons, interneurons and motor neurons. That the gut does not work without the ENS can be made as an absolute statement. This is apparent in its absence in terminal regions of the large intestine in Hirschsprung's disease in humans and animals where it is reflected by dysfunctional motility, failure of defecation and proximal fecal compaction within a proximal megacolon. Autoimmune ablation of the ENS in the lower esophageal sphincter underlies the pathophysiology of achalasia. Furthermore, neuropathic degeneration of ENS neurons in irritable bowel syndrome, other functional gastrointestinal disorders, intestinal pseudoobstruction, Chagas disease, paraneoplastic syndrome and enteric ganglionitis, underlies the morbidity associated with these disorders. The impact of these clinical disorders on quality of life and cost of health care is a reminder of the importance of the ENS for a normally functioning gut. Moreover, our incomplete understanding of the pathobiology of these disorders highlights a need for research directed to expansion of current knowledge of the neurobiology of the ENS at all levels of organization from the cellular biology of individual neurons to the biophysics of integrated networks to whole organ behavior. Investigation of the normal and disordered ENS and its interactions with the central nervous system is a branch of neurogastroenterology. Neurogastroenterology is a scientific and clinical subspecialty of gastroenterology that deals with the neural mechanisms that influence function of the digestive tract and that underlie projection of conscious sensations to the gut |
Analysis |
enteric nervous system |
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central nervous system |
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neurogastroenterology |
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functional gastrointestinal disorders |
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irritable bowel syndrome |
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Hirschsprung's disease |
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abdominal pain |
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diarrhea |
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constipation |
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neurogenesis |
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neural plasticity |
Notes |
Title from Web page (viewed Oct. 3, 2011) |
Bibliography |
Includes bibliographical references (pages 123-160) |
Subject |
Autonomic ganglia.
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Gastrointestinal system -- Innervation.
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Enteric Nervous System
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Ganglia, Autonomic
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Gastrointestinal Tract -- innervation
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MEDICAL -- Nutrition.
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Autonomic ganglia
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Gastrointestinal system -- Innervation
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Form |
Electronic book
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ISBN |
9781615043408 |
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1615043403 |
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