Enterochromaffin cell

About: Enterochromaffin cell is a research topic. Over the lifetime, 1198 publications have been published within this topic receiving 51601 citations. The topic is also known as: enterochromaffin cells & Kulchitsky cells.

Ghrelin, a novel growth hormone-releasing acylated peptide, is synthesized in a distinct endocrine cell type in the gastrointestinal tracts of rats and humans.

Abstract: Ghrelin, a novel GH-releasing acylated peptide, was recently isolated from rat stomach. It stimulated the release of GH from the anterior pituitary through the GH secretagogue receptor (GHS-R). Ghrelin messenger RNA and the peptide are present in rat stomach, but its cellular source has yet to be determined. Using two different antibodies against the N- and C-terminal regions of rat ghrelin, we identified ghrelin-producing cells in the gastrointestinal tracts of rats and humans by light and electron microscopic immunohistochemistry and in situ hybridization combined with immunohistochemistry. Ghrelin-immunoreactive cells, which are not enterochromaffin-like cells, D cells, or enterochromaffin cells, accounted for about 20% of the endocrine cell population in rat and human oxyntic glands. Rat ghrelin was present in round, compact, electron-dense granules compatible with those of X/A-like cells whose hormonal product and physiological functions have not previously been clarified. The localization, population, and ultrastructural features of ghrelin-producing cells (Gr cells) indicate that they are X/A-like cells. Ghrelin also was found in enteric endocrine cells of rats and humans. Using two RIAs for the N- and C-terminal regions of ghrelin, we determined its content in the rat gastrointestinal tract. Rat ghrelin was present from the stomach to the colon, with the highest content being in the gastric fundus. Messenger RNAs of ghrelin and GHS-R also were found in these organs. Ghrelin probably functions not only in the control of GH secretion, but also in the regulation of diverse processes of the digestive system. Our findings provide clues to additional, as yet undefined, physiological functions of this novel gastrointestinal hormone.

Principles and clinical implications of the brain-gut-enteric microbiota axis.

Abstract: While bidirectional brain-gut interactions are well known mechanisms for the regulation of gut function in both healthy and diseased states, a role of the enteric flora--including both commensal and pathogenic organisms--in these interactions has only been recognized in the past few years. The brain can influence commensal organisms (enteric microbiota) indirectly, via changes in gastrointestinal motility and secretion, and intestinal permeability, or directly, via signaling molecules released into the gut lumen from cells in the lamina propria (enterochromaffin cells, neurons, immune cells). Communication from enteric microbiota to the host can occur via multiple mechanisms, including epithelial-cell, receptor-mediated signaling and, when intestinal permeability is increased, through direct stimulation of host cells in the lamina propria. Enterochromaffin cells are important bidirectional transducers that regulate communication between the gut lumen and the nervous system. Vagal, afferent innervation of enterochromaffin cells provides a direct pathway for enterochromaffin-cell signaling to neuronal circuits, which may have an important role in pain and immune-response modulation, control of background emotions and other homeostatic functions. Disruption of the bidirectional interactions between the enteric microbiota and the nervous system may be involved in the pathophysiology of acute and chronic gastrointestinal disease states, including functional and inflammatory bowel disorders.

The migration of neural crest cells to the wall of the digestive tract in avian embryo.

Abstract: Isotopic and isochronic grafts of quail neural primordium in chick embryos have been made. Due to the particular structure of their nuclei, quail cells can be distinguished from chick cells and so be used as natural markers to study the migration of neural crest cells. We have been able to demonstrate by this technique that the parasympathetic enteric ganglion cells arise from two different levels of the embryonic neural axis which correspond to the vagal and lumbo-sacral parasympathetic centres. The main source of the enteric neuroblasts is located at the level of the somites 1–7. It gives rise to ganglion cells which migrate in the whole gut including the large intestine and rectum. The other region from which enteric neuroblasts originate is situated behind the level of the 28th somite and gives rise only to some post-umbilical gut ganglion cells. In this region of the intestine the ganglia are made up of a mixture of cells arising from the vagal and the lumbo-sacral levels of the neural axis. The part of the neural primordium between the 8th and the 28th somite does not participate in the formation of the enteric ganglia. The chronology of the enteric neuroblast migration has been studied. Most cells of vagal origin leave the neural crest before the 13-somite stage but the migration lasts sometimes until after the 16-somite stage. Those cells which have to reach the hind-gut level accomplish a long-term migration which can be evaluated at 6 days or more. The presumptive neuroblasts of lumbo-sacral origin are not found in the hind-gut before the 7th day of incubation. In our experiments we have never observed the migration of any quail cells into the endoderm of the chick host embryo. Therefore we consider that enterochromaffin cells of the digestive epithelium are not derived from the levels of the neural crest concerned in these experiments (i.e. rhombencephalic and medullary Anlagen).