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The gastrointestinal tract is a long, muscular tube responsible for the digestion of food, assimilation of nutrients and elimination of waste. This is achieved by secretion of digestive enzymes and absorption from the intestinal lumen, with different regions playing specific roles in the processing of specific nutrients. These regions come into play sequentially as ingested material is moved along the length of the GI tract by contractions of the muscle layers. In some regions like the oesophagus transit it rapid and measured in seconds while in others like the colon transit is measured in hours and even days, commensurate with the relative slow fermentation that takes place in the large bowel. An hierarchy of controls, neural and endocrine, serve to regulate the various cellular targets that exist in the gut wall. These include muscle cells for contraction and epithelial cells for secretion and absorption. However, there are complex interactions between these digestive mechanisms and other mechanisms that regulate blood flow, immune function, endocrine secretion and food intake. These ensure a fine balance between the ostensibly conflicting tasks of digestion and absorption and protection from potentially harmful ingested materials. They match assimilation of nutrients with hunger and satiety and they ensure that regions of the GI tract that are meters apart work together in a coordinated fashion to match these diverse functions to the digestive needs of the individual. This ebook will provide an overview of the neural mechanisms that control gastrointestinal function. Table of Contents: Neural Control of Gastrointestinal Function / Cells and Tissues / Enteric Nervous System / From Gut to CNS: Extrinsic Sensory Innervation / Sympathetic Innervation of the Gut / Parasympathetic Innervation of the Gut / Integration of Function / References
Nearly 30 years ago, a number of scientists working on the Enteric Nervous System (ENS) gathered at Flinders University, in Adelaide, Australia to discuss the advances and future of their research. It was a friendly and stimulating meeting, attended by most of the major players, in what was to become the discipline of ‘Neurogastroenterology'. In 2014, the main Australasian Neuroscience Society meeting was held in Adelaide, Australia, providing the perfect opportunity to recreate a follow-up ENS meeting. As such, the ‘ENS II 2014 meeting’ aimed to identify how far the field of enteric neuroscience had developed, where the future was heading, and what technological advances had been made to address current and future unresolved questions. 30 speakers from around the world were invited to give talks and revisit the original expectations, the advances made since, and the future directions of ENS research. These discussions included three generations of investigators from 7 different countries. This publication represents the majority of proceedings from the ‘The Enteric Nervous System II 2014’ conference, which was held on February 1st - 2nd 2014 at the National Wine Centre of Australia, Adelaide. This meeting was an Official satellite meeting of the 34th Annual Meeting of Australasian Neuroscience Society, which was also held in Adelaide. The 20 contributions contained within this submission are from international researchers in the field of the ENS, who reviewed the advances made since the first meeting in the early 1980s and summarizes the present and future perspectives of neuro-gastroenterology. Some colleagues could not attend but did send greetings and their messages are included in these proceedings.
On July 9-10, 2014, the Institute of Medicine's Food Forum hosted a public workshop to explore emerging and rapidly developing research on relationships among the brain, the digestive system, and eating behavior. Drawing on expertise from the fields of nutrition and food science, animal and human physiology and behavior, and psychology and psychiatry as well as related fields, the purpose of the workshop was to (1) review current knowledge on the relationship between the brain and eating behavior, explore the interaction between the brain and the digestive system, and consider what is known about the brain's role in eating patterns and consumer choice; (2) evaluate current methods used to determine the impact of food on brain activity and eating behavior; and (3) identify gaps in knowledge and articulate a theoretical framework for future research. Relationships among the Brain, the Digestive System, and Eating Behavior summarizes the presentations and discussion of the workshop.
This book offers one of the most comprehensive reviews in the field of gastrointestinal (GI) physiology, guiding readers on a journey through the complete digestive tract, while also highlighting related organs and glandular systems. It is not solely limited to organ system physiology, and related disciplines like anatomy and histology, but also examines the molecular and cellular processes that keep the digestive system running. As such, the book provides extensive information on the molecular, cellular, tissue, organ, and system levels of functions in the GI system. Chapters on the roles of the gut as an endocrine, exocrine and neural organ, as well as its microbiome functions, broaden readers’ understanding of the multi-organ networks in the human body. To help illustrate the interconnections between the physiological concepts, principles and clinical presentations, it outlines clinical examples such as pathologies that link basic science with clinical practice in special “clinical correlates” sections. Covering both traditional and contemporary topics, it is a valuable resource for biomedical students, as well as healthcare and scientific professionals.
The kidney is innervated with efferent sympathetic nerve fibers reaching the renal vasculature, the tubules, the juxtaglomerular granular cells, and the renal pelvic wall. The renal sensory nerves are mainly found in the renal pelvic wall. Increases in efferent renal sympathetic nerve activity reduce renal blood flow and urinary sodium excretion by activation of α1-adrenoceptors and increase renin secretion rate by activation of β1-adrenoceptors. In response to normal physiological stimulation, changes in efferent renal sympathetic nerve activity contribute importantly to homeostatic regulation of sodium and water balance. The renal mechanosensory nerves are activated by stretch of the renal pelvic tissue produced by increases in renal pelvic tissue of a magnitude that may occur during increased urine flow rate. Activation of the sensory nerves elicits an inhibitory renorenal reflex response consisting of decreases in efferent renal sympathetic nerve activity leading to natriuresis. Increasing efferent sympathetic nerve activity increases afferent renal nerve activity which, in turn, decreases efferent renal sympathetic nerve activity by activation of the renorenal reflexes. Thus, activation of the afferent renal nerves buffers changes in efferent renal sympathetic nerve activity in the overall goal of maintaining sodium balance. In pathological conditions of sodium retention, impairment of the inhibitory renorenal reflexes contributes to an inappropriately increased efferent renal sympathetic nerve activity in the presence of sodium retention. In states of renal disease or injury, there is a shift from inhibitory to excitatory reflexes originating in the kidney. Studies in essential hypertensive patients have shown that renal denervation results in long-term reduction in arterial pressure, suggesting an important role for the efferent and afferent renal nerves in hypertension. Table of Contents: Part I: Efferent Renal Sympathetic Nerves / Introduction / Neuroanatomy / Neural Control of Renal Hemodynamics / Neural Control of Renal Tubular Function / Neural Control of Renin Secretion Rate / Part II: Afferent Renal Sensory Nerves / Introduction / Neuroanatomy / Renorenal Reflexes / Mechanisms Involved in the Activation of Afferent Renal Sensory Nerves / Part III: Pathophysiological States / Efferent Renal Sympathetic Nerves / Afferent Renal Sensory Nerves / Conclusions / References
The enteric nervous system (ENS) is a complex neural network embedded in the gut wall that orchestrates the reflex behaviors of the intestine. The ENS is often referred to as the “little brain” in the gut because the ENS is more similar in size, complexity and autonomy to the central nervous system (CNS) than other components of the autonomic nervous system. Like the brain, the ENS is composed of neurons that are surrounded by glial cells. Enteric glia are a unique type of peripheral glia that are similar to astrocytes of the CNS. Yet enteric glial cells also differ from astrocytes in many important ways. The roles of enteric glial cell populations in the gut are beginning to come to light and recent evidence implicates enteric glia in almost every aspect of gastrointestinal physiology and pathophysiology. However, elucidating the exact mechanisms by which enteric glia influence gastrointestinal physiology and identifying how those roles are altered during gastrointestinal pathophysiology remain areas of intense research. The purpose of this e-book is to provide an introduction to enteric glial cells and to act as a resource for ongoing studies on this fascinating population of glia. Table of Contents: Introduction / A Historical Perspective on Enteric Glia / Enteric Glia: The Astroglia of the Gut / Molecular Composition of Enteric Glia / Development of Enteric Glia / Functional Roles of Enteric Glia / Enteric Glia and Disease Processes in the Gut / Concluding Remarks / References / Author Biography
As aging trends in the United States and Europe in particular are strongly suggestive of increasingly older society, it would be prudent for health care providers to better prepare for such changes. By including physiology, disease, nutrition, pharmacology, pathology, radiology and other relevant associated topics, Geriatric Gastroenterology fills the void in the literature for a volume devoted specifically to gastrointestinal illness in the elderly. This unique volume includes provision of training for current and future generations of physicians to deal with the health problems of older adults. It will also serve as a comprehensive guide to practicing physicians for ease of reference. Relevant to the geriatric age group, the volume covers epidemiology, physiology of aging, gastrointestinal physiology, pharmacology, radiology, pathology, motility disorders, luminal disorders, hepato-biliary disease, systemic manifestations, neoplastic disorders, gastrointestinal bleeding, cancer and medication related interactions and adverse events, all extremely common in older adults; these are often hard to evaluate and judge, especially considering the complex aging physiology. All have become important components of modern medicine. Special emphasis is be given to nutrition and related disorders. Capsule endoscopy and its utility in the geriatric population is also covered. Presented in simple, easy to read style, the volume includes numerous tables, figures and key points enabling ease of understanding. Chapters on imaging and pathology are profusely illustrated. All chapters are written by specialists and include up to date scientific information. Geriatric Gastroenterology is of great utility to residents in internal medicine, fellows in gastroenterology and geriatric medicine as well as gastroenterologists, geriatricians and practicing physicians including primary care physicians caring for older adults.
The long tube that makes up the gastrointestinal tract is composed of a variety of tissue types and is the largest internal organ of the body. Its main function is to digest food and absorb the released nutrients. Furthermore, it is subdivided into functionally distinct regions that each mediate one of a variety of actions upon the food consumed, including ingestion, propulsion, secretion, digestion, absorption and expulsion. Autonomic neuronal circuitry is intimately involved in controlling many of these multiple functions of the gut, making it an appealing subject for the study of neuroscientists. This book reviews the state of current knowledge on the innervation of the gut by the enteric nervous system, and its interface with the extrinsic innervation, from a number of different perspectives, with the aim of providing a comprehensive and accessible account of the subject.
Three distinct types of contractions perform colonic motility functions. Rhythmic phasic contractions (RPCs) cause slow net distal propulsion with extensive mixing/turning over. Infrequently occurring giant migrating contractions (GMCs) produce mass movements. Tonic contractions aid RPCs in their motor function. The spatiotemporal patterns of these contractions differ markedly. The amplitude and distance of propagation of a GMC are several-fold larger than those of an RPC. The enteric neurons and smooth muscle cells are the core regulators of all three types of contractions. The regulation of contractions by these mechanisms is modifiable by extrinsic factors: CNS, autonomic neurons, hormones, inflammatory mediators, and stress mediators. Only the GMCs produce descending inhibition, which accommodates the large bolus being propelled without increasing muscle tone. The strong compression of the colon wall generates afferent signals that are below nociceptive threshold in healthy subjects. However, these signals become nociceptive; if the amplitudes of GMCs increase, afferent nerves become hypersensitive, or descending inhibition is impaired. The GMCs also provide the force for rapid propulsion of feces and descending inhibition to relax the internal anal sphincter during defecation. The dysregulation of GMCs is a major factor in colonic motility disorders: irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and diverticular disease (DD). Frequent mass movements by GMCs cause diarrhea in diarrhea predominant IBS, IBD, and DD, while a decrease in the frequency of GMCs causes constipation. The GMCs generate the afferent signals for intermittent short-lived episodes of abdominal cramping in these disorders. Epigenetic dysregulation due to adverse events in early life is one of the major factors in generating the symptoms of IBS in adulthood.