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Meier-Ruge, William A., and Luzia A. Brunner. "Morphometric Assessment of Hirschsprung's Disease: Associated Hypoganglionosis of the Colonic Myenteric Plexus." Pediatric and Developmental Pathology 4, no. 1 (January 2001): 53–61. http://dx.doi.org/10.1007/s100240010115.
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At present, there are no generally acceptable criteria for the evaluation of hypoganglionosis of the myenteric plexus. The aim of this morphometrical investigation was to examine the most important quantitative characteristics of hypoganglionosis. Colon specimens from 35 children with Hirschsprung's disease were assessed morphometrically. Twenty specimens with Hirschsprung's disease and proximal hypoganglionosis of the myenteric plexus were compared with 15 specimens with Hirschsprung's disease and normal innervation in the proximal myenteric plexus. All native surgical specimens were caudocranial coiled and sectioned in a cryostat. Nerve cells and ganglia were selectively stained with an enzyme-histochemical lactic dehydrogenase reaction. Morphometric measurements were done with an optic-electronic image analysis system. Hirschsprung's disease–associated hypoganglionosis of the myenteric plexus is characterized by a significant decrease in ganglion cross-sectional area (-56.2%) and in plexus area per mm colon (-53.5%). Together with these data, an increase in ganglion distance (+20%) was also determined, and the number of nerve cells per mm colon was decreased by −25.5%. The decrease in ganglion area and in the number of nerve cells per mm colon in the myenteric plexus proved to be the most characteristic parameters of a hypoganglionosis.
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Hagger, Robert, Sussan Gharaie, Caroline Finlayson, and Devinder Kumar. "Regional and transmural density of interstitial cells of Cajal in human colon and rectum." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 6 (December 1, 1998): G1309—G1316. http://dx.doi.org/10.1152/ajpgi.1998.275.6.g1309.
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The interstitial cells of Cajal (ICC) are thought to play an important role in the control of gut motility. The regional and transmural pattern of distribution of ICC in the normal human colon and rectum was evaluated with immunohistochemistry using an anti-c- kit antibody. The transmural distribution of ICC was constant throughout the whole colon, the density of ICC was significantly greater at the myenteric plexus than at either the longitudinal or circular muscle layers, and in the rectum the transmural distribution was more even. Regionally, at the myenteric plexus, the transverse colon had a significantly greater density of ICC compared with the right colon ( P = 0.038), left colon ( P = 0.006), and rectum ( P = 0.008). The pattern of distribution of ICC identified in this study is consistent with the proposed roles of ICC as colorectal pacemakers, intermediaries of the neural control of muscle activity, and coordinators of colorectal muscle activity. The highest density of ICC was at the myenteric plexus of the transverse colon, which is the proposed region of pacemaking activity.
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Adad, Sheila Jorge, Renata Margarida Etchebehere, and Alessandro Adad Jammal. "BLOOD VESSELS IN GANGLIA IN HUMAN ESOPHAGUS MIGHT EXPLAIN THE HIGHER FREQUENCY OF MEGAESOPHAGUS COMPARED WITH MEGACOLON." Revista do Instituto de Medicina Tropical de São Paulo 56, no. 6 (December 2014): 529–32. http://dx.doi.org/10.1590/s0036-46652014000600013.
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This study aimed to determine the existence of blood vessels within ganglia of the myenteric plexus of the human esophagus and colon. At necropsy, 15 stillborns, newborns and children up to two years of age, with no gastrointestinal disorders, were examined. Rings of the esophagus and colon were analyzed and then fixed in formalin and processed for paraffin. Histological sections were stained by hematoxylin-eosin, Giemsa and immunohistochemistry for the characterization of endothelial cells, using antibodies for anti-factor VIII and CD31. Blood vessels were identified within the ganglia of the myenteric plexus of the esophagus, and no blood vessels were found in any ganglia of the colon. It was concluded that the ganglia of the myenteric plexus of the esophagus are vascularized, while the ganglia of the colon are avascular. Vascularization within the esophageal ganglia could facilitate the entrance of infectious agents, as well as the development of inflammatory responses (ganglionitis) and denervation, as found in Chagas disease and idiopathic achalasia. This could explain the higher frequency of megaesophagus compared with megacolon.
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Baruhee, Divya. "Developing myenteric plexus in human foetal colon." Journal of the Anatomical Society of India 66 (August 2017): S86. http://dx.doi.org/10.1016/j.jasi.2017.08.270.
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Berezin, I., J. D. Huizinga, and E. E. Daniel. "Structural characterization of interstitial cells of Cajal in myenteric plexus and muscle layers of canine colon." Canadian Journal of Physiology and Pharmacology 68, no. 11 (November 1, 1990): 1419–31. http://dx.doi.org/10.1139/y90-216.
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We have carried out a detailed ultrastructural study of the interstitial cells near the myenteric plexus of the canine colon and defined the structural characteristics which distinguish them from other resident non-neural cells. We have also examined the interconnections of these interstitial cells with nerves, the longitudinal muscle, and the circular muscle. In addition, we sought connections between interstitial cells of the myenteric plexus and those described earlier at the inner border of the circular muscle in proximal and distal colon. The interstitial cells of the myenteric plexus were structurally distinctive, and made gap junctions with one another and occasionally with smooth muscle. There seemed to be two subsets of these interstitial cells, one associated with the longitudinal muscle and the other with the circular muscle. Cells of both subsets were often close (≤20 nm) to nerve profiles. The interstitial cells near the longitudinal muscle layer penetrated slightly into the muscle layer, but those near the circular muscle did not and neither set contacted the other. Moveover, interstitial cells of Cajal located near the myenteric plexus were never observed to contact those at the inner border of circular muscle. The interstitial cells of Cajal at the canine colon myenteric plexus are structurally organized to provide independent pacemaking activities for the longitudinal and adjacent circular muscle. Their dense innervation suggests that they mediate neural modulation of intestinal pacemaker activities. Moreover, they lack direct contacts with the interstitial cell network at the inner border of circular muscle, which is essential for the primary pacemaking activity of circular muscle. The structural organization of interstitial cells in canine colon is consistent with their proposed role in pacemaking activity of the two muscle layers.Key words: pacemakers, neuromodulation, interstitial cells of Cajal.
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Bistoletti, Michela, Giovanni Micheloni, Nicolò Baranzini, Annalisa Bosi, Andrea Conti, Viviana Filpa, Cristina Pirrone, et al. "Homeoprotein OTX1 and OTX2 involvement in rat myenteric neuron adaptation after DNBS-induced colitis." PeerJ 8 (February 13, 2020): e8442. http://dx.doi.org/10.7717/peerj.8442.
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Background Inflammatory bowel diseases are associated with remodeling of neuronal circuitries within the enteric nervous system, occurring also at sites distant from the acute site of inflammation and underlying disturbed intestinal functions. Homeoproteins orthodenticle OTX1 and OTX2 are neuronal transcription factors participating to adaptation during inflammation and underlying tumor growth both in the central nervous system and in the periphery. In this study, we evaluated OTX1 and OTX2 expression in the rat small intestine and distal colon myenteric plexus after intrarectal dinitro-benzene sulfonic (DNBS) acid-induced colitis. Methods OTX1 and OTX2 distribution was immunohistochemically investigated in longitudinal muscle myenteric plexus (LMMP)-whole mount preparations. mRNAs and protein levels of both OTX1 and OTX2 were evaluated by qRT-PCR and Western blotting in LMMPs. Results DNBS-treatment induced major gross morphology and histological alterations in the distal colon, while the number of myenteric neurons was significantly reduced both in the small intestine and colon. mRNA levels of the inflammatory markers, TNFα, pro-IL1β, IL6, HIF1α and VEGFα and myeloperoxidase activity raised in both regions. In both small intestine and colon, an anti-OTX1 antibody labeled a small percentage of myenteric neurons, and prevalently enteric glial cells, as evidenced by co-staining with the glial marker S100β. OTX2 immunoreactivity was present only in myenteric neurons and was highly co-localized with neuronal nitric oxide synthase. Both in the small intestine and distal colon, the number of OTX1- and OTX2-immunoreactive myenteric neurons significantly increased after DNBS treatment. In these conditions, OTX1 immunostaining was highly superimposable with inducible nitric oxide synthase in both regions. OTX1 and OTX2 mRNA and protein levels significantly enhanced in LMMP preparations of both regions after DNBS treatment. Conclusions These data suggest that colitis up-regulates OTX1 and OTX2 in myenteric plexus both on site and distantly from the injury, potentially participating to inflammatory-related myenteric ganglia remodeling processes involving nitrergic transmission.
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Wester, T., D. S. O’Briain, and P. Puri. "Notable postnatal alterations in the myenteric plexus of normal human bowel." Gut 44, no. 5 (May 1, 1999): 666–74. http://dx.doi.org/10.1136/gut.44.5.666.
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BACKGROUNDNitric oxide is the most important transmitter in non-adrenergic non-cholinergic nerves in the human gastrointestinal tract. Impaired nitrergic innervation has been described in Hirschsprung’s disease, hypertrophic pyloric stenosis, and intestinal neuronal dysplasia (IND). Recent findings indicate that hyperganglionosis, one of the major criteria of IND, is age dependent. However, information is scanty regarding the neurone density in normal human bowel in the paediatric age group.AIMSTo determine neurone density, morphology, and nitric oxide synthase distribution of the normal myenteric plexus at different ages during infancy and childhood.METHODSSpecimens were obtained from small bowel and colon in 20 children, aged one day to 15 years, at postmortem examination. Whole mount preparations were made of the myenteric plexus, which were subsequently stained using NADPH diaphorase histochemistry (identical to nitric oxide synthase) and cuprolinic blue (a general neuronal marker). The morphology of the myenteric plexus was described and the neurone density estimated.RESULTSThe myenteric plexus meshwork becomes less dense during the first years of life. The density of ganglion cells in the myenteric plexus decreases significantly with age during the first three to four years of life. The NADPH diaphorase positive (nitrergic) subpopulation represents about 34% of all neurones in the myenteric plexus.CONCLUSIONSThe notable decrease in neurone density in the myenteric plexus during the first years of life indicates that development is still an ongoing process in the postnatal enteric nervous system. Applied to the clinical situation, this implies that interpretation of enteric nervous system pathology is dependent on the age of the patient.
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Wiese, J. J., A. Fascì, A. A. Kühl, B. Siegmund, M. S. Prüß, and M. Schumann. "P061 Immune cell infiltrations of myenteric plexus in IBD – characterization and implications." Journal of Crohn's and Colitis 15, Supplement_1 (May 1, 2021): S167—S168. http://dx.doi.org/10.1093/ecco-jcc/jjab076.190.
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Abstract Background IBD frequently causes chronic abdominal pain and visceral hypersensitivity. To understand development of pain in IBD in more detail, we analyzed the inflammatory infiltration of the enteric nervous system (ENS). A crucial signaling point for pain transmission is the myenteric plexus situated in the smooth muscle layer of the colon wall. We investigated (i) the immune cell infiltration within the myenteric plexus, (ii) neuronal cell survival and (iii) expression of neurotransmitters by immunostaining in surgical colonic samples from patients with Crohn′s disease (CD) or ulcerative colitis (UC). Methods FFPE material from surgeries (ileocecal resections and colectomies) was collected from 12 UC, nine CD and 11 patients that received surgeries for non-inflammatory reasons (controls). Immune cell composition, neurotransmitter expression and cell survival were analyzed by quantifying immune cell infiltration of the myenteric ganglia in immunohistochemistry sections. Immune cells within the myenteric plexus were defined as intraganglionar cells. The neurotransmitters CGRP and substance P as well as annexin V as a cell death marker were quantified based on their expression within the myenteric ganglia. Results CD3+CD4+ intraganglionar T-cells (216 ± 44 cells/mm²) were found to be increased for CD myenteric plexus compared to controls (79 ± 35 cells/mm²) (p=0.04) (see Fig. 1). For CD and UC, the cell counts of CD3+CD8+ lymphocytes infiltrating the myenteric plexus were significantly increased (controls: 39 ± 18 cells/mm², CD: 281 ± 105 cells/mm² (p=0.0004), UC: 177 ± 59 cells/mm² (p=0.04), Intraganglionar Foxp3+ T-cells were not significantly changed. Intraganglionar CD163+ and CD68+ monocytes were increased in CD (CD68+ monocytes: control: 377 ± 50 cells/mm², CD: 1278 ± 264 cells/mm², p=0.002 and CD163+ monocytes: control: 501 ± 97 cells/mm², CD: 963 ± 236 cells/mm², p=0.04). Expression levels of the neurotransmitter CGRP were found to be increased for UC myenteric plexus (control: 1.8 ± 0.2 units of intensity, UC: 2.8 ± 0.2 units of intensity, p=0.005). Substance P was found to be reduced in the myenteric plexus of CD patients if compared to controls (control: 2.1 ± 0.1 units of intensity, CD: 1.5 ± 0.2 units of intensity, p=0.007). UC myenteric plexus showed more annexin V-positive cells than control patients. Conclusion The intraganglionar immune cell composition of myenteric plexus in IBD comprises CD3+CD4+, CD3+CD8 T-cells in UC and CD3+CD4+, CD3+CD8+ and CD3+Foxp3+ T-cells as well as CD68+ and CD163+ monocytes in CD. In UC myenteric ganglia levels of the neurotransmitter CGRP are increased whereas substance P expression is reduced in CD. UC-affected myenteric plexus show increased levels of apoptosis in comparison to controls.
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Stojanovska, Vanesa, Rachel M. McQuade, Sarah Miller, and Kulmira Nurgali. "Effects of Oxaliplatin Treatment on the Myenteric Plexus Innervation and Glia in the Murine Distal Colon." Journal of Histochemistry & Cytochemistry 66, no. 10 (May 9, 2018): 723–36. http://dx.doi.org/10.1369/0022155418774755.
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Oxaliplatin (platinum-based chemotherapeutic agent) is a first-line treatment of colorectal malignancies; its use associates with peripheral neuropathies and gastrointestinal side effects. These gastrointestinal dysfunctions might be due to toxic effects of oxaliplatin on the intestinal innervation and glia. Male Balb/c mice received intraperitoneal injections of sterile water or oxaliplatin (3 mg/kg/d) triweekly for 2 weeks. Colon tissues were collected for immunohistochemical assessment at day 14. The density of sensory, adrenergic, and cholinergic nerve fibers labeled with calcitonin gene-related peptide (CGRP), tyrosine hydroxylase (TH), and vesicular acetylcholine transporter (VAChT), respectively, was assessed within the myenteric plexus of the distal colon. The number and proportion of excitatory neurons immunoreactive (IR) against choline acetyltransferase (ChAT) were counted, and the density of glial subpopulations was determined by using antibodies specific for glial fibrillary acidic protein (GFAP) and s100β protein. Oxaliplatin treatment induced significant reduction of sensory and adrenergic innervations, as well as the total number and proportion of ChAT-IR neurons, and GFAP-IR glia, but increased s100β expression within the myenteric plexus of the distal colon. Treatment with oxaliplatin significantly alters nerve fibers and glial cells in the colonic myenteric plexus, which could contribute to long-term gastrointestinal side effects following chemotherapeutic treatment.
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Inoue, T., T. Okasora, and E. Okamoto. "Effect on muscarinic acetylcholine receptors after experimental neuronal ablation in rat colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 6 (December 1, 1995): G940—G944. http://dx.doi.org/10.1152/ajpgi.1995.269.6.g940.
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The etiology of denervation hypersensitivity was studied using a rat model. Degeneration of the myenteric plexus was produced by direct application of 0.1% benzalkonium chloride to the serosal surface of the distal colon. Thirty days later, the treated group was compared with a control group undergoing a sham operation. The treated group showed that the decreased number of ganglion cells of the myenteric plexus on routine stain and acetylcholinesterase staining demonstrated the myenteric plexus in the treated group diminished acetylcholinesterase activity. Methacholine (1%), a muscarinic agonist, increased intraluminal pressure in treated but not control rats. The dose-response curve of colonic muscle strips to oxotremorine showed a shift to the left, indicating greater sensitivity, in the treated bowel, with a 50% effective dose (ED50) of 2.5 x 10(-8) in treated muscle and 2.2 x 10(-7) in controls. Binding studies using [3H]quinuclidinyl benzilate ([3H]QNB) showed that the specific maximal binding (Bmax) for [3H]QNB was greater in treated than in untreated animals (228 +/- 26.1 and 135 +/- 42.9 fmol/mg protein, respectively; P < 0.01), even though the dissociation constants (Kd) were the same (0.398 +/- 0.083 and 0.406 +/- 0.065). These findings show that acquired denervation hypersensitivity in this model is due to an increase in the number of muscarinic acetylcholine receptors.
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Bódi, Nikolett, Lalitha Chandrakumar, Afnan al Doghmi, Diána Mezei, Zita Szalai, Bence Pál Barta, János Balázs, and Mária Bagyánszki. "Intestinal Region-Specific and Layer-Dependent Induction of TNFα in Rats with Streptozotocin-Induced Diabetes and after Insulin Replacement." Cells 10, no. 9 (September 13, 2021): 2410. http://dx.doi.org/10.3390/cells10092410.
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Tumour necrosis factor alpha (TNFα) is essential in neuroinflammatory modulation. Therefore, the goal of this study is to reveal the effects of chronic hyperglycaemia and insulin treatment on TNFα expression in different gut segments and intestinal wall layers. TNFα expression was mapped by fluorescent immunohistochemistry and quantitative immunogold electron microscopy in myenteric ganglia of duodenum, ileum and colon. Tissue TNFα levels were measured by enzyme-linked immunosorbent assays in muscle/myenteric plexus-containing (MUSCLE-MP) and mucosa/submucosa/submucous plexus-containing (MUC-SUBMUC-SP) homogenates. Increasing density of TNFα-labelling gold particles is observed in myenteric ganglia from proximal to distal segments and TNFα tissue levels are much more elevated in MUSCLE-MP homogenates than in MUC-SUBMUC-SP samples in healthy controls. In the diabetics, the number of TNFα gold labels is significantly increased in the duodenum, decreased in the colon and remained unchanged in the ileal ganglia, while insulin does not prevent these diabetes-related TNFα changes. TNFα tissue concentration is also increased in MUSCLE-MP homogenates of diabetic duodenum, while decreased in MUC-SUBMUC-SP samples of diabetic ileum and colon. These findings support that type 1 diabetes has region-specific and intestinal layer-dependent effects on TNFα expression, contributing to the regional damage of myenteric neurons and their intestinal milieu.
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Bódi, Nikolett, Abigél Egyed-Kolumbán, Benita Onhausz, Bence Pál Barta, Afnan AL Doghmi, János Balázs, Zita Szalai, and Mária Bagyánszki. "Intestinal Region-Dependent Alterations of Toll-Like Receptor 4 Expression in Myenteric Neurons of Type 1 Diabetic Rats." Biomedicines 11, no. 1 (January 4, 2023): 129. http://dx.doi.org/10.3390/biomedicines11010129.
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Toll-like receptor 4 (TLR4) can activate pro-inflammatory cascades in the gastrointestinal tract. Our aim was to determine TLR4 expression in myenteric neurons of different gut regions using a type 1 diabetic model. Ten weeks after the onset of hyperglycemia, myenteric whole-mount preparations from the duodenum, ileum and colon of streptozotocin-induced diabetic, insulin-treated diabetic and control rats were prepared for TLR4/peripherin double-labelling fluorescent immunohistochemistry. Immunogold electron microscopy was applied to evaluate TLR4 expression in the myenteric perikaryon and neuropil. Tissue TLR4 levels were measured by enzyme-linked immunosorbent assay. In controls, the number and proportion of the TLR4-immunoreactive myenteric neurons showed an increasing tendency to aboral direction. These values were significantly higher in diabetics compared to controls in the duodenum and ileum, but were significantly lower in the colon. In diabetics, the distribution of TLR4-labelling gold particles between the perikaryon and neuropil of myenteric neurons varied in a different way by intestinal segment. TLR4 tissue concentration changed only in the diabetic duodenum, and it decreased in muscle/myenteric plexus-containing homogenates, while it increased in mucosa/submucosa/submucous plexus-containing samples relative to controls. Insulin had beneficial effects on TLR4 expression. These findings support that chronic hyperglycemia has segment-specific effects on TLR4 expression, contributing to gastrointestinal disorders in diabetic patients.
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Huizinga, Jan D., Carlos Barajas-Lopez, and Edwin Chow. "Generation of spiking activity in circular muscle cells of the canine colon." Canadian Journal of Physiology and Pharmacology 65, no. 10 (October 1, 1987): 2147–50. http://dx.doi.org/10.1139/y87-337.
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Spontaneous and current-induced electrical activity was recorded intracellularly to resolve the controversy whether or not the circular muscle layer of the colon generates spiking activity. Particularly in the first hour after mounting the tissue in the organ bath, spikes were recorded at both the submucosal and the myenteric plexus side of the muscle layer. Spikes were seen as part of the slow wave upstroke in the submucosal surface cells, and spikes occurred both at the upstroke potential and superimposed on the plateau potential in myenteric plexus surface cells. Spikes increased the force of contraction. The study supports earlier claims using extracellular recording techniques that circular muscle cells generate spiking activity, particularly in the presence of depolarizing stimuli, and that spikes contribute to contractile activity.
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Hasler, W. L., S. Kurosawa, and O. Y. Chung. "Regional cholinergic differences between distal and proximal colonic myenteric plexus." American Journal of Physiology-Gastrointestinal and Liver Physiology 258, no. 3 (March 1, 1990): G404—G410. http://dx.doi.org/10.1152/ajpgi.1990.258.3.g404.
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We investigated differences in myogenic and neural response of proximal vs. distal guinea pig colon in longitudinal and circular muscle. Spontaneous phasic contractions were more intense in distal colon in both layers. Phasic contractile frequency was also greater in distal colon in both layers. In both longitudinal and circular muscle, acetylcholine induced greater contractions in distal than in proximal colon (maximal response: longitudinal, 7.00 +/- 1.04 X 10(4) vs. 3.50 +/- 0.49 X 10(4) N/m2; circular, 3.29 +/- 0.82 X 10(4) vs. 8.92 +/- 1.30 X 10(3) N/m2). Compared with proximal colon, electric field stimulation induced greater atropine-sensitive contractions in distal colon in both muscle layers (maximal response: longitudinal, 4.22 +/- 0.53 X 10(4) vs. 7.53 +/- 1.97 X 10(3) N/m2; circular, 2.14 +/- 0.79 X 10(3) vs. -5.28 +/- 2.04 X 10(2) N/m2). In contrast, there were no regional differences in atropine-insensitive relaxations. Veratridine (10(-5) M) stimulated greater [3H]acetylcholine release from distal longitudinal muscle-myenteric plexus than from proximal preparations (11.44 +/- 2.03 vs. 5.84 +/- 1.26% of total tissue radioactivity). These data suggest the greater contractile responses in the distal colon are because of enhanced cholinergic response to neural stimuli and increased muscle sensitivity to acetylcholine, whereas there are no differences in the inhibitory responses to neural stimuli.
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Luo, Jialie, Haitang Li, Dongsheng Shu, and Hongzhen Hu. "Calcium Sensing Receptor in Rat Myenteric Plexus of Colon." Gastroenterology 140, no. 5 (May 2011): S—521. http://dx.doi.org/10.1016/s0016-5085(11)62163-x.
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Yakabi, Seiichi, Lixin Wang, Hiroshi Karasawa, Pu-Qing Yuan, Kazuhiko Koike, Koji Yakabi, and Yvette Taché. "VIP is involved in peripheral CRF-induced stimulation of propulsive colonic motor function and diarrhea in male rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 314, no. 5 (May 1, 2018): G610—G622. http://dx.doi.org/10.1152/ajpgi.00308.2017.
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We investigated whether vasoactive intestinal peptide (VIP) and/or prostaglandins contribute to peripheral corticotropin-releasing factor (CRF)-induced CRF1 receptor-mediated stimulation of colonic motor function and diarrhea in rats. The VIP antagonist, [4Cl-D-Phe6, Leu17]VIP injected intraperitoneally completely prevented CRF (10 µg/kg ip)-induced fecal output and diarrhea occurring within the first hour after injection, whereas pretreatment with the prostaglandins synthesis inhibitor, indomethacin, had no effect. In submucosal plexus neurons, CRF induced significant c-Fos expression most prominently in the terminal ileum compared with duodenum and jejunum, whereas no c-Fos was observed in the proximal colon. c-Fos expression in ileal submucosa was colocalized in 93.4% of VIP-positive neurons and 31.1% of non-VIP-labeled neurons. CRF1 receptor immunoreactivity was found on the VIP neurons. In myenteric neurons, CRF induced only a few c-Fos-positive neurons in the ileum and a robust expression in the proximal colon (17.5 ± 2.4 vs. 0.4 ± 0.3 cells/ganglion in vehicle). The VIP antagonist prevented intraperitoneal CRF-induced c-Fos induction in the ileal submucosal plexus and proximal colon myenteric plexus. At 60 min after injection, CRF decreased VIP levels in the terminal ileum compared with saline (0.8 ± 0.3 vs. 2.5 ± 0.7 ng/g), whereas VIP mRNA level detected by qPCR was not changed. These data indicate that intraperitoneal CRF activates intestinal submucosal VIP neurons most prominently in the ileum and myenteric neurons in the colon. It also implicates VIP signaling as part of underlying mechanisms driving the acute colonic secretomotor response to a peripheral injection of CRF, whereas prostaglandins do not play a role. NEW & NOTEWORTHY Corticotropin-releasing factor (CRF) in the gut plays a physiological role in the stimulation of lower gut secretomotor function induced by stress. We showed that vasoactive intestinal peptide (VIP)-immunoreactive neurons in the ileal submucosal plexus expressed CRF1 receptor and were prominently activated by CRF, unlike colonic submucosal neurons. VIP antagonist abrogated CRF-induced ileal submucosal and colonic myenteric activation along with functional responses (defecation and diarrhea). These data point to VIP signaling in ileum and colon as downstream effectors of CRF.
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Tjwa, Eric T. T. L., Joelle M. Bradley, Catherine M. Keenan, Alfons B. A. Kroese, and Keith A. Sharkey. "Interleukin-1β activates specific populations of enteric neurons and enteric glia in the guinea pig ileum and colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 285, no. 6 (December 2003): G1268—G1276. http://dx.doi.org/10.1152/ajpgi.00073.2003.
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Fos expression was used to assess whether the proinflammatory cytokine interleukin-1β (IL-1β) activated specific, chemically coded neuronal populations in isolated preparations of guinea pig ileum and colon. Whether the effects of IL-1β were mediated through a prostaglandin pathway and whether IL-1β induced the expression of cyclooxygenase (COX)-2 was also examined. Single- and double-labeling immunohistochemistry was used after treatment of isolated tissues with IL-1β (0.1-10 ng/ml). IL-1β induced Fos expression in enteric neurons and also in enteric glia in the ileum and colon. For enteric neurons, activation was concentration-dependent and sensitive to indomethacin, in both the myenteric and submucosal plexuses in both regions of the gut. The maximum proportion of activated neurons differed between the ileal (∼15%) and colonic (∼42%) myenteric and ileal (∼60%) and colonic (∼75%) submucosal plexuses. The majority of neurons activated in the myenteric plexus of the ileum expressed nitric oxide synthase (NOS) or enkephalin immunoreactivity. In the colon, activated myenteric neurons expressed NOS. In the submucosal plexus of both regions of the gut, the majority of activated neurons were vasoactive intestinal polypeptide (VIP) immunoreactive. After treatment with IL-1β, COX-2 immunoreactivity was detected in the wall of the gut in both neurons and nonneuronal cells. In conclusion, we have found that the proinflammatory cytokine IL-1β specifically activates certain neurochemically defined neural pathways and that these changes may lead to disturbances in motility observed in the inflamed bowel.
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Frieling, T., H. J. Cooke, and J. D. Wood. "Electrophysiological properties of neurons in submucosal ganglia of guinea pig distal colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 6 (June 1, 1991): G835—G841. http://dx.doi.org/10.1152/ajpgi.1991.260.6.g835.
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Intracellular recording methods were used in vitro to study the electrophysiological behavior of neurons in ganglia of the submucosal plexus in the distal colon of the guinea pig. The results revealed subpopulations of submucosal ganglion cells that corresponded to the AH/type 2, S/type 1, type 3, and type 4 subpopulations found elsewhere in the intestine. Electrical behavior of colonic submucosal neurons differed from the myenteric plexus of the colon, rectum, and stomach and the small intestinal submucosal plexus mainly in the relative proportions of the different subpopulations. Regional differences in this respect may be a reflection of functional specialization in the diverse regions of the alimentary canal.
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Matsumoto, Kenjiro, Emi Kurosawa, Hiroyuki Terui, Takuji Hosoya, Kimihito Tashima, Toshihiko Murayama, John V. Priestley, and Syunji Horie. "Localization of TRPV1 and contractile effect of capsaicin in mouse large intestine: high abundance and sensitivity in rectum and distal colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 2 (August 2009): G348—G360. http://dx.doi.org/10.1152/ajpgi.90578.2008.
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We investigated immunohistochemical differences in the distribution of TRPV1 channels and the contractile effects of capsaicin on smooth muscle in the mouse rectum and distal, transverse, and proximal colon. In the immunohistochemical study, TRPV1 immunoreactivity was found in the mucosa, submucosal, and muscle layers and myenteric plexus. Large numbers of TRPV1-immunoreactive axons were observed in the rectum and distal colon. In contrast, TRPV1-positive axons were sparsely distributed in the transverse and proximal colon. The density of TRPV1-immunoreactive axons in the rectum and distal colon was much higher than those in the transverse and proximal colon. Axons double labeled with TRPV1 and protein gene product (PGP) 9.5 were detected in the myenteric plexus, but PGP 9.5-immunoreactive cell bodies did not colocalize with TRPV1. In motor function studies, capsaicin induced a fast transient contraction, followed by a large long-lasting contraction in the rectum and distal colon, whereas in the transverse and proximal colon only the transient contraction was observed. The capsaicin-induced transient contraction from the proximal colon to the rectum was moderately inhibited by an NK1or NK2receptor antagonist. The capsaicin-induced long-lasting contraction in the rectum and distal colon was markedly inhibited by an NK2antagonist, but not by an NK1antagonist. The present results suggest that TRPV1 channels located on the rectum and distal colon play a major role in the motor function in the large intestine.
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Smith, T. K., J. B. Reed, and K. M. Sanders. "Electrical pacemakers of canine proximal colon are functionally innervated by inhibitory motor neurons." American Journal of Physiology-Cell Physiology 256, no. 3 (March 1, 1989): C466—C477. http://dx.doi.org/10.1152/ajpcell.1989.256.3.c466.
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Pacemaker activity in the canine proximal colon occurs at the submucosal and myenteric borders of the circular layer [Am. J. Physiol. 252 (Cell Physiol. 21): C215-C224 and C290-C299, 1987]. The present study investigated the neural regulation of rhythmic electrical activity. Spontaneous inhibitory junction potentials (IJPs) were observed in intracellular recordings from circular muscle cells near the myenteric border. The amplitudes of these events decayed with distance through the circular layer. Stimulation at the myenteric plexus surface evoked IJPs that mimicked the spontaneous events. Stimulation at the submucosal surface evoked IJPs in adjacent cells that were of shorter duration and of different waveform than myenteric IJPs. Amplitudes of IJPs evoked by stimulation near either surface decayed with distance from the site of stimulation. The decay functions for IJPs were essentially identical to the decay of spontaneous slow waves or myenteric potential oscillations. Spontaneous and evoked IJPs affected the amplitudes, durations, and patterns of ongoing rhythmic electrical activity. The data suggest that myenteric and submucosal pacemaker populations may be innervated by different populations of inhibitory nerve fibers. Innervation appears to be heterogeneous with dense populations of inhibitory nerve fibers predominantly located in the pacemaker regions. Neural regulations of pacemaker activity influences rhythmic electrical activity throughout the muscularis.
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Feng, Mei, Junfang Qin, Chao Wang, Yanfang Ye, Shuanglian Wang, Dongping Xie, Paulus S. Wang, and Chuanyong Liu. "Estradiol upregulates the expression of oxytocin receptor in colon in rats." American Journal of Physiology-Endocrinology and Metabolism 296, no. 5 (May 2009): E1059—E1066. http://dx.doi.org/10.1152/ajpendo.90609.2008.
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The study was designed to investigate the effect of estradiol on the excitatory effect of oxytocin (OT) on colon motility. Female Wistar rats were used, and some of them were ovariectomized (OVX) and treated with vehicle or estradiol (E2). A plastic balloon made of condom was inserted into colon to monitor the change of colonic pressure in vivo. Longitudinal muscle strips of distal colon were prepared to monitor the spontaneous contraction of colon in vitro. Expression of OT receptor (OTR) was investigated by Western blot analysis. Expression of OTR mRNA was detected by RT-PCR. Immunohistochemistry was used to locate OTR. In OVX rats, pretreatment of E2 (4–100 μg/kg sc) dose-dependently increased the excitatory effect of OT on colon motility both in vivo and in vitro and increased the expression of OTR and OTR mRNA in colon. Systemic administration of OT excited the colon motility in vivo in rats at perioda of proestrus and estrus but did not influence it at diestrus period, when the concentration of plasma E2 was lowest in the estrous cycle. Pretreatment of atosiban, the specific OTR antagonist, and TTX, the blocker of voltage-dependent sodium channel on nerve fiber, attenuated the excitatory effect of OT on colon motility. OTR was located in myenteric plexus of colon. These results suggested that E2 increased the excitatory effect of OT on colon motility by upregulating the expression of OTR in myenteric plexus.
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Farraway, L., A. K. Ball, and J. D. Huizinga. "Intercellular metabolic coupling in canine colon musculature." American Journal of Physiology-Cell Physiology 268, no. 6 (June 1, 1995): C1492—C1502. http://dx.doi.org/10.1152/ajpcell.1995.268.6.c1492.
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Intercellular communication within the musculature of the canine colon was studied by examining the results of neurobiotin diffusion after injection of the tracer into smooth muscle cells at different locations within the muscle layer. Circular muscle at the submucosal surface, circular muscle adjacent to the myenteric plexus, and longitudinal muscle demonstrated different degrees of time-dependent tracer spread. At the submucosal surface, tracer spread was rapid, extensive, and unimpeded by connective tissue septa. At the myenteric side, tracer spread was also extensive but was much slower and confined to bundles of cells bordered by septa. In contrast to previous studies that suggest an absence of gap junctions at the myenteric side of the circular muscle, the neurobiotin spread indicates full metabolic coupling of all circular smooth muscle cells. Furthermore, in contrast to the belief that longitudinal muscle is completely devoid of gap junctions, tracer spread occurred between cells in this layer, although neurobiotin diffusion was very limited, nonuniform, and slow. In each area of the musculature studied, tracer spread was inhibited by octanol. When very long injection and wait times were implemented at the submucosal surface of the circular muscle, neurobiotin was observed to cross septa through the network of interstitial cells of Cajal, indicating that it is this network that provides communication between lamellae.
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Miampamba, Marcel, Celine Maillot, Mulugeta Million, and Yvette Taché. "Peripheral CRF activates myenteric neurons in the proximal colon through CRF1 receptor in conscious rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 282, no. 5 (May 1, 2002): G857—G865. http://dx.doi.org/10.1152/ajpgi.00434.2001.
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Corticotropin-releasing factor (CRF) injected peripherally induces clustered spike-burst activity in the proximal colon through CRF1 receptors in rats. We investigated the effect of intraperitoneal CRF on proximal colon ganglionic myenteric cell activity in conscious rats using Fos immunohistochemistry on the colonic longitudinal muscle/myenteric plexus whole mount preparation. In vehicle-pretreated rats, there were only a few Fos immunoreactive (IR) cells per ganglion (1.2 ± 0.6). CRF (10 μg/kg ip) induced Fos expression in 19.6 ± 2.1 cells/ganglion. The CRF1/CRF2 antagonist astressin (33 μg/kg ip) and the selective CRF1 antagonist CP-154,526 (20 mg/kg sc) prevented intraperitoneal CRF-induced Fos expression in the proximal colon (number of Fos-IR cells/ganglion: 2.7 ± 1.2 and 1.0 ± 1.0, respectively), whereas atropine (1 mg/kg sc) had no effect. Double labeling of Fos with protein gene product 9.5 revealed the neuronal identity of activated cells that were encircled by varicose fibers immunoreactive to vesicular acetylcholine transporter. Fos immunoreactivity was mainly present in choline acetyltransferase-IR nerve cell bodies but not in the NADPH-diaphorase-positive cells. These results indicate that peripheral CRF activates myenteric cholinergic neurons in the proximal colon through CRF1 receptor.
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Mandic, Predrag, Tatjana Filipovic, Milos Gasic, Natasa Djukic-Macut, Milan Filipovic, and Ivan Bogosavljevic. "Quantitative morphometric analysis of the myenteric nervous plexus ganglion structures along the human digestive tract." Vojnosanitetski pregled 73, no. 6 (2016): 559–65. http://dx.doi.org/10.2298/vsp141231046m.
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Background/Aim. All the functions of the digestive system are controlled, guided and initiated by the autonomic nervous system. A special part of this system placed in the wall of the gastrointestinal tract is known as the enteric or metasympathetic nervous system. The aim of this study was to analyse myenteric nervous plexus in different parts of the digestive tract. Methods. We examined the myenteric nervous plexus of the esophagus, stomach, duodenum, jejunum, ileum, transverse colon and rectum in tissue samples taken from 30 cadavers of persons aged 20-84 years. After standard histological processing sections were stained with hematoxylineosin, cresyl violet (CV) and AgNO3 method. Multipurpose test system M42 was used in morphometric analysis. The results were analyzed by t-test and analysis of variance. Results. The number of neurons per cm2 surface was the lowest in the esophagus (2.045 ? 310.30) and the largest in the duodenum (65,511 ? 5,639). The statistical processing showed significant differences (p < 0.001) in the number of neurons between the esophagus and all other parts of the digestive tract. The maximal value of the average surface of the myenteric nervous plexus neurons was observed in the esophagus (588.93 ? 30.45 ?m2) and the lowest in the stomach (296.46 ? 22.53 ?m2). Conclusion. There are differences in the number of ganglion cells among different parts of the human digestive tract. The differences range from a few to several tens of thousands of neuron/cm2. The myenteric nervous plexus of the esophagus was characterized by a significantly smaller number of neurons but their bodies and nuclei are significantly larger compared to other parts of the digestive tract.
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Spencer, Nick J., Sarah J. Nicholas, Lucy Robinson, Melinda Kyloh, Nicholas Flack, Simon J. Brookes, Vladimir P. Zagorodnyuk, and Damien J. Keating. "Mechanisms underlying distension-evoked peristalsis in guinea pig distal colon: is there a role for enterochromaffin cells?" American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 3 (September 2011): G519—G527. http://dx.doi.org/10.1152/ajpgi.00101.2011.
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The mechanisms underlying distension-evoked peristalsis in the colon are incompletely understood. It is well known that, following colonic distension, 5-hydroxytryptamine (5-HT) is released from enterochromaffin (EC) cells in the intestinal mucosa. It is also known that exogenous 5-HT can stimulate peristalsis. These observations have led some investigators to propose that endogenous 5-HT release from EC cells might be involved in the initiation of colonic peristalsis, following distension. However, because no direct evidence exists to support this hypothesis, the aim of this study was to determine directly whether release of 5-HT from EC cells was required for distension-evoked colonic peristalsis. Real-time amperometric recordings of 5-HT release and video imaging of colonic wall movements were performed on isolated segments of guinea pig distal colon, during distension-evoked peristalsis. Amperometric recordings revealed basal and transient release of 5-HT from EC cells before and during the initiation of peristalsis, respectively. However, removal of mucosa (and submucosal plexus) abolished 5-HT release but did not inhibit the initiation of peristalsis nor prevent the propagation of fecal pellets or intraluminal fluid. Maintained colonic distension by fecal pellets induced repetitive peristaltic waves, whose intrinsic frequency was also unaffected by removal of the submucosal plexus and mucosa, although their propagation velocities were slower. In conclusion, the mechanoreceptors and sensory neurons activated by radial distension to initiate peristalsis lie in the myenteric plexus and/or muscularis externa, and their activation does not require the submucosal plexus, release of 5-HT from EC cells, nor the presence of the mucosa. The propagation of peristalsis and propulsion of liquid or solid content along the colon is entrained by activity within the myenteric plexus and/or muscularis externa and does not require sensory feedback from the mucosa, nor neural inputs arising from submucosal ganglia.
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Trout, S. J. "Assessment of acetylcholine release from myenteric plexus of guinea-pig colon." Journal of Pharmacy and Pharmacology 38, no. 4 (April 1986): 310–12. http://dx.doi.org/10.1111/j.2042-7158.1986.tb04575.x.
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Chumasov, Evgenii I., Pavel N. Romashchenko, Nicolay A. Maistrenko, Vadim B. Samedov, Elena S. Petrova, and Dmitry E. Korzhevskii. "Pathohistological study of the ganglion plexuses of the sigmoid colon in patients with chronic slow-transit constipation." Bulletin of the Russian Military Medical Academy 23, no. 3 (November 3, 2021): 117–24. http://dx.doi.org/10.17816/brmma75673.
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The morphological study of the resected sections of the colon obtained at the S.P. Fedorov Department of Faculty Surgery of S.M. Kirov Military Medical Academy, as a result of surgical treatment of patients with severe chronic slow-transit constipation, included an assessment of the changes in the structures of ganglion plexuses. Three cases were considered (women, aged 3740 years). Various degrees of pathological changes were detected in the ganglion plexuses (Auerbach and Meissner) of the sigmoid colon from patients with chronic slow-transit constipation using Nissls toluidine blue staining. In all cases, reactive, dystrophic, severe degenerative-necrotic changes of ganglion cells, as well as the details of their death, were described in detail. Along with pathological changes in nerve cells in the myenteric nerve plexus and gliosis, features of neuronglial relationships were described, and the death of ganglion cells in the human colon with the active participation of specialized astrocyte-like glial cells was also established for the first time. In the third case, a pattern of pronounced dysplasia and dysgangliogenesis was revealed in the myenteric ganglion plexus of the sigmoid colon, and the presence of diffuse lymphmonocytic infiltrates was noted in the circular muscle layer. Pathological changes in the enteral nervous system in chronic slow-transit constipation reflect neuropathy, which can serve as the main cause of impaired intestinal functions and of some symptoms.
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Côbo, Eliângela de Castro, Thales Parenti Silveira, Adilha Misson Micheletti, Eduardo Crema, and Sheila Jorge Adad. "Research onTrypanosoma cruziand Analysis of Inflammatory Infiltrate in Esophagus and Colon from Chronic Chagasic Patients with and without Mega." Journal of Tropical Medicine 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/232646.
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To compare parasitism and inflammatory process in esophagus and colon from chronic chagasic patients, immunohistochemistry was carried out to research forT. cruziand to evaluate the inflammatory infiltrate in the muscular and myenteric plexus in 39 esophagi (20 with and 19 without megaesophagus) and 50 colons (25 with and 25 without megacolon). The frequency ofT. cruziin megaesophagus was 20%, and in megacolon it was 4%. No amastigotes were found in organs without mega; considering the total of esophagi (with and without mega), the frequency ofT. cruziwould be 10% and 2% in the colon. Myositis and ganglionitis were more frequent and intense in organs with mega compared to those without mega, and in esophagus compared to colon. Qualitatively, inflammatory infiltration in esophagus and colon, with or without mega, was similar, consisting predominantly of T lymphocytes (CD3+), scarce macrophages (CD68+), and rare B lymphocytes (CD20+).
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Wang, Y. F., and E. E. Daniel. "Gap junctions in gastrointestinal muscle contain multiple connexins." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 2 (August 1, 2001): G533—G543. http://dx.doi.org/10.1152/ajpgi.2001.281.2.g533.
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In the canine gastrointestinal tract, the roles that gap junctions play in pacemaking and neurotransmission are unclear. Using antibodies to connexin (Cx)43, Cx45, and Cx40, we determined the distribution of these connexins. Cx43 was present in all locations where structural gap junctions occur. Cx40 was also widely distributed in the circular muscle of the lower esophageal sphincter (LES), stomach, and ileum. Cx45 was sparsely distributed in circular muscle of the LES. In the interstitial cells of Cajal (ICC) networks of myenteric plexus, in the deep muscular and submuscular plexuses, sparse Cx45 and Cx40 immunoreactivity was present. In colon, immunoreactivity was found only in the myenteric and submuscular plexus and nearby circular muscle cells. No immunoreactivity was found in sites lacking structural gap junctions (longitudinal muscle, inner circular muscle of the intestine, and most circular muscle of the colon). Studies of colocalization of connexins suggested that in the ICC networks, some colocalization of Cx43 with Cx40 and/or Cx45 occurred. Thus gap junctions in canine intestine may be heterotypic or heteromeric and have different conductance properties in different regions based on different connexin compositions.
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Kimura, Takazumi, Tomofumi Amano, Hirotsugu Uehara, Hajime Ariga, Tsuyoshi Ishida, Akira Torii, Hisao Tajiri, Kei Matsueda, and Shigeru Yamato. "Urocortin I is present in the enteric nervous system and exerts an excitatory effect via cholinergic and serotonergic pathways in the rat colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 4 (October 2007): G903—G910. http://dx.doi.org/10.1152/ajpgi.00066.2007.
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Corticotropin-releasing factor (CRF) and urocortin I (UcnI) have been shown to accelerate colonic transit after central nervous system (CNS) or peripheral administration, but the mechanism of their peripheral effect on colonic motor function has not been fully investigated. Furthermore, the localization of UcnI in the enteric nervous system (ENS) of the colon is unknown. We investigated the effect of CRF and UcnI on colonic motor function and examined the localization of CRF, UcnI, CRF receptors, choline acetyltransferase (ChAT), and 5-HT. Isometric tension of rat colonic muscle strips was measured. The effect of CRF, UcnI on phasic contractions, and electrical field stimulation (EFS)-induced off-contractions were examined. The effects of UcnI on both types of contraction were also studied in the presence of antalarmin, astressin2-B, tetrodotoxin (TTX), atropine, and 5-HT antagonists. The localizations of CRF, UcnI, CRF receptors, ChAT, and 5-HT in the colon were investigated by immunohistochemistry. CRF and UcnI increased both contractions dose dependently. UcnI exerted a more potent effect than CRF. Antalarmin, TTX, atropine, and 5-HT antagonists abolished the contractile effects of UcnI. CRF and UcnI were observed in the neuronal cells of the myenteric plexus. UcnI and ChAT, as well as UcnI and 5-HT, were colocalized in some of the neuronal cells of the myenteric plexus. This study demonstrated that CRF and UcnI act on the ENS and increase colonic contractility by enhancing cholinergic and serotonergic neurotransmission. These peptides are present in myenteric neurons. CRF and, perhaps, to a greater extent, UcnI appear to act as neuromodulators in the ENS of the rat colon.
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Barajas-Lopez, C., and J. D. Huizinga. "Different mechanisms of contraction generation in circular muscle of canine colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 3 (March 1, 1989): G570—G580. http://dx.doi.org/10.1152/ajpgi.1989.256.3.g570.
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Smooth muscle cells from the circular muscle layer of the dog colon showed a mechanical threshold of -44 mV. No gradient in mechanical threshold was measured between the cells from the submucosal and myenteric plexus surface. The threshold was passed during the upstroke and the plateau phase of the spontaneous slow-wave activity from cells at the submucosal surface and by spike potentials occurring mainly in cells at the myenteric plexus surface and sporadically in cells at the submucosal surface. Carbachol-induced specific changes in electrical and mechanical activities that were inhibited by calcium influx blockade are as follows: 1) increase in slow-wave duration; 2) decrease in plateau potential; 3) enhancement of spiking activity; and 4) increase in contractility. This indicates that calcium influx is significantly increased in the presence of carbachol in cells at both surfaces of the circular muscle layer. The increase in calcium influx could be the result of a direct action by carbachol on the calcium conductance and/or could be mediated by a decrease in outward current. The latter is suggested by the carbachol-induced membrane depolarization associated with an increase in the input resistance, which were both methoxyverapamil insensitive. The results show that an excitatory stimulus can generate contraction of the circular muscle through different electrophysiological activities. In addition, the patterns of spontaneous electrical activity and the different responses to carbachol stimulation provide further information about the heterogeneous nature of the electrical activities within the colonic circular muscle layer.
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Porter, A. J., D. A. Wattchow, S. J. H. Brookes, and M. Costa. "Cholinergic and nitrergic interneurones in the myenteric plexus of the human colon." Gut 51, no. 1 (July 1, 2002): 70–75. http://dx.doi.org/10.1136/gut.51.1.70.
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Johannes Rumessen, Jüri, Jean-Marie Vanderwinden, Helle Rasmussen, Alastair Hansen, and Thomas Horn. "Ultrastructure of interstitial cells of Cajal in myenteric plexus of human colon." Cell and Tissue Research 337, no. 2 (June 9, 2009): 197–212. http://dx.doi.org/10.1007/s00441-009-0818-6.
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Furukawa, K., G. S. Taylor, and R. A. Bywater. "An intracellular study of myenteric neurons in the mouse colon." Journal of Neurophysiology 55, no. 6 (June 1, 1986): 1395–406. http://dx.doi.org/10.1152/jn.1986.55.6.1395.
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Intracellular recordings have been made in vitro from the myenteric neurons of the distal colon of normal littermates of the piebald-lethal mouse. Out of a total of 90 neurons, 82 were classified as S/type 1 cells and 8 as AH/type 2 cells. Seventy-eight out of 82 S cells showed spontaneous fast excitatory postsynaptic potentials (EPSPs) sensitive to d-tubocurarine (dTC, 280 microM), and 22 S cells showed spontaneous action potentials (APs). Six S cells and 1 AH cell showed spontaneous nonnicotinic slow depolarizations associated with an increase in the input resistance of the cells; during the spontaneous slow depolarization in the S cells there was an increase in the frequency of nicotinic fast EPSPs and APs. Three S cells showed spontaneously occurring regular oscillations of the membrane potential (approximately mV in amplitude and approximately 4/min). Transmural nerve stimulation produced fast EPSPs with a wide range of latencies (3 ms to 20 s) in S cells; the fast EPSPs were blocked by dTC (280 microM) or solutions containing low Ca2+ (0.25 mM) and high Mg2+ (12 mM) but not by atropine (ATR, 14 microM). Single or repetitive transmural stimulation produced slow EPSPs in 24 S cells and 3 AH cells; these were not blocked by dTC (280 microM) nor ATR (14 microM). During the slow EPSPs there was an increase in the input resistance of the cells. In those S cells that showed slow EPSPs there were many long-latency fast EPSPs; long-latency fast EPSPs were also observed in 11 other S cells that did not show a slow EPSP following repetitive transmural nerve stimulation. Long-latency fast EPSPs may be related to the firing of other neurons during their slow EPSPs. The myenteric neurons in the mouse colon have similar properties to the myenteric neurons in the guinea pig small intestine. However, the colonic myenteric neurons show more ongoing synaptic activity and more prolonged activity after nerve stimulation than myenteric neurons in the guinea pig small intestine. This activity may be due to regional differences, species differences, or preparation differences (in this study the myenteric plexus was adherent to the underlying circular muscle layer).
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Sant'Ana, Débora de Mello Gonçales, Sônia Lucy Molinari, and Marcílio Hubner Miranda-Neto. "Effects of protein and vitamin B deficiency on blood parameters and myenteric neurons of the colon of rats." Arquivos de Neuro-Psiquiatria 59, no. 3A (September 2001): 493–98. http://dx.doi.org/10.1590/s0004-282x2001000400003.
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The aims of this work were to evaluate the effects of the deficient ingestion of protein and vitamin B on the biochemical and hematologic parameters and on the NADH- and NADPH-diaphorase positive myenteric neurons. The control animals (n=10) received commercial chow and the experimental rats (n=10) received chow with protein level reduced to 8% during 120 days. At the time of killing blood was collected for assessment of the blood and hematologic parameters and the ascending colon for quantitative analysis of the neurons of the myenteric plexus. It was observed that the reduction of the protein level to 8% coupled to the reduction of the levels of vitamin B in adult rats neither led to qualitative or quantitative changes on red or white blood cells, nor decreased globulin levels, induced the formation of edema or gave rise to clinical signs typical of protein or vitamin B deficiency. On the other hand, the experimental protocol led to less weight gain, change on the body composition with fat deposition; decrease of the values of serum total protein and albumin; reduction of the area of colon and density of nitrergic and NADH-diaphorase myenteric neurons inferior to the expected.
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Broad, John, Victor W. S. Kung, Alexandra Palmer, Shezan Elahi, Azadeh Karami, Taher Darreh-Shori, Shafi Ahmed, et al. "Changes in neuromuscular structure and functions of human colon during ageing are region-dependent." Gut 68, no. 7 (September 18, 2018): 1210–23. http://dx.doi.org/10.1136/gutjnl-2018-316279.
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ObjectiveTo determine if human colonic neuromuscular functions decline with increasing age.DesignLooking for non-specific changes in neuromuscular function, a standard burst of electrical field stimulation (EFS) was used to evoke neuronally mediated (cholinergic/nitrergic) contractions/relaxations in ex vivomuscle strips of human ascending and descending colon, aged 35–91 years (macroscopically normal tissue; 239 patients undergoing cancer resection). Then, to understand mechanisms of change, numbers and phenotype of myenteric neurons (30 306 neurons stained with different markers), densities of intramuscular nerve fibres (51 patients in total) and pathways involved in functional changes were systematically investigated (by immunohistochemistry and use of pharmacological tools) in elderly (≥70 years) and adult (35–60 years) groups.ResultsWith increasing age, EFS was more likely to evoke muscle relaxation in ascending colon instead of contraction (linear regression: n=109, slope 0.49%±0.21%/year, 95% CI), generally uninfluenced by comorbidity or use of medications. Similar changes were absent in descending colon. In the elderly, overall numbers of myenteric and neuronal nitric oxide synthase-immunoreactive neurons and intramuscular nerve densities were unchanged in ascending and descending colon, compared with adults. In elderly ascending, not descending, colon numbers of cell bodies exhibiting choline acetyltransferase immunoreactivity increased compared with adults (5.0±0.6 vs 2.4±0.3 neurons/mm myenteric plexus, p=0.04). Cholinergically mediated contractions were smaller in elderly ascending colon compared with adults (2.1±0.4 and 4.1±1.1 g-tension/g-tissue during EFS; n=25/14; p=0.04); there were no changes in nitrergic function or in ability of the muscle to contract/relax. Similar changes were absent in descending colon.ConclusionIn ascending not descending colon, ageing impairs cholinergic function.
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Berezin, Irene, Jan D. Huizinga, Laura Farraway, and Edwin E. Daniel. "Innervation of interstitial cells of Cajal by vasoactive intestinal polypeptide containing nerves in canine colon." Canadian Journal of Physiology and Pharmacology 68, no. 7 (July 1, 1990): 922–32. http://dx.doi.org/10.1139/y90-141.
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The hypothesis was tested, through structural and functional studies, that interstitial cells of Cajal receive and can respond to direct innervation from nerves containing the vasoactive intestinal polypeptide neuromediator. The submucosal network of interstitial cells of Cajal has been postulated to provide pacemaking activity for the circular muscle and to be involved in neurotransmission from noradrenergic, noncholinergic nerves for which vasoactive intestinal polypeptide is a putative mediator. The distribution of vasoactive intestinal polypeptide and substance P immunoreactive material in nerve profiles of the enteric nervous system of the canine colon was examined. In addition, electrophysiological studies were done on the interstitial cells bordering the submucosal side of the circular muscle layer after they were electrically isolated using heptanol. The vasoactive intestinal polypeptide immunoreactivity, located exclusively in nerve large granular vesicles, was found throughout the enteric nervous system (myenteric plexus, submucous plexus, and circular muscle – submucosa interface). The highest proportion (38% compared with 22–24%) of profiles of large granular vesicles with vasoactive intestinal polypeptide immunoreactivity was found in nerve profiles of the circular muscle – submucosa interface. In contrast, substance P immunoreactivity was found in nerve profiles of myenteric plexus (33% of large granular vesicles were positive) but not associated with submucosal interstitial cell nerve network. The vasoactive intestinal polypeptide hyperpolarized interstitial cells by 9 mV when electrically isolated by 1 mM heptanol and markedly reduced (about 50%) their input membrane resistance. We conclude that the distribution of vasoactive intestinal polypeptide immunoreactivity and its action are consistent with a postulated role of the interstitial cells as a major site of neurally mediated inhibition of colonic pacemaker activity.Key words: enteric nervous system, interstitial cells of Cajal, inhibitory junction potential, nonadrenergic noncholinergic nerves.
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Spencer, Nick J., Grant W. Hennig, and Terence K. Smith. "Electrical rhythmicity and spread of action potentials in longitudinal muscle of guinea pig distal colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 282, no. 5 (May 1, 2002): G904—G917. http://dx.doi.org/10.1152/ajpgi.00345.2001.
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Using simultaneous intracellular recordings, we have characterized 1) electrical activity in the longitudinal muscle (LM) of isolated segments of guinea pig distal colon free to contract spontaneously and 2) extent of propagation of spontaneous action potentials around the circumference of the colon. In all animals, rhythmical spontaneous depolarizations (SDs) were recorded that are usually associated with the generation of action potentials. Recordings from pairs of LM cells, separated by 100 μm in the circumferential axis, revealed that each action potential was phase locked at the two electrodes (mean propagation velocity: 3 mm/s). However, at an increased electrode separation distance of 1 mm circumferentially, action potentials and SDs became increasingly uncoordinated at the two recording sites. No SDs or action potentials ever propagated from one circumferential edge to the other (i.e., 13 mm apart). When LM strips were separated from the myenteric plexus and circular muscle, rhythmically firing SDs and action potentials were still recorded. Atropine (1 μM) or tetrodotoxin (1 μM) either reduced the frequency of SDs or temporily abolished activity, whereas nifedipine (1 μM) always abolished SDs and action potentials. Kit-positive interstitial cells of Cajal were present at the level of the myenteric plexus and circular and longitudinal muscle. In summary, SDs and action potentials in LM propagate over discrete localized zones, usually <1 mm around the circumference of the colon. Furthermore, in contrast to the classic slow wave, rhythmic depolarizations in LM appear to be generated by an intrinsic property of the smooth muscle itself and are critically dependent on opening of L-type Ca2+ channels.
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Quobatari, Ammar, and John W. Wiley. "Diabetic enteric neuropathy is associated with apoptosis in the rat colon myenteric plexus." Gastroenterology 118, no. 4 (April 2000): A384. http://dx.doi.org/10.1016/s0016-5085(00)83645-8.
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Fellig, Y., A. Vromen, R. Udassin, H. R. Freund, and M. Hanani. "The morphology of myenteric plexus of the human colon is altered with age." Gastroenterology 114 (April 1998): A1386—A1387. http://dx.doi.org/10.1016/s0016-5085(98)85633-3.
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Huang, Zitong, Lu Liao, Zhesheng Wang, Yulin Lu, Weiming Yan, Hongying Cao, and Bo Tan. "An efficient approach for wholemount preparation of the myenteric plexus of rat colon." Journal of Neuroscience Methods 348 (January 2021): 109012. http://dx.doi.org/10.1016/j.jneumeth.2020.109012.
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Buckinx, R., S. Van Remoortel, C. Van den Haute, Z. Debyser, S. Waddington, and J. P. Timmermans. "rAAV transduction in the myenteric and submucous plexus of mouse ileum and colon." Autonomic Neuroscience 192 (November 2015): 61. http://dx.doi.org/10.1016/j.autneu.2015.07.026.
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Christensen, James, and Gary A. Rick. "Distribution of myelinated nerves in ascending nerves and myenteric plexus of cat colon." American Journal of Anatomy 178, no. 3 (March 1987): 250–58. http://dx.doi.org/10.1002/aja.1001780306.
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Leite-Mello, Emeri V. S., Sandra Regina Stabille, and Marcílio H. Miranda-Neto. "Effect of maternal protein deprivation on morphological and quantitative aspects of the myenteric plexus neurons of proximal colon in rats." Arquivos de Neuro-Psiquiatria 55, no. 1 (1997): 106–13. http://dx.doi.org/10.1590/s0004-282x1997000100017.
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We have studied the morphological and quantitative aspects of the myenteric plexus neurons of the proximal colon in rats (Rattus norvegicus of Wistar strain) submitted to a protein deprivation during prenatal and lactation periods. Twenty pregnant dams were divided in four groups labeled according to the kind of nourishment they were given: Group NN, normal diet; Group DN, low protein diet during prenatal period, and normal diet during lactation period; Group ND, normal diet during prenatal period, and low protein diet during lactation period; Group DD, low protein diet during prenatal and lactation periods. Histological analyses were developed with proximal colon segments using the haematoxylin and eosin staining method. Membrane preparations were stained by Giemsa's method. The statistical analysis has demonstrated no significant difference among the means of neurons found in the four studied groups. It was noticed that the animals under protein deprivation during prenatal and lactation periods presented greater quantity of large and strongly basophilic myenteric neurons. This suggests that neurons have accumulated protein in the cytoplasm.
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Storr, M., A. Sibaev, G. Marsicano, B. Lutz, V. Schusdziarra, J. P. Timmermans, and H. D. Allescher. "Cannabinoid receptor type 1 modulates excitatory and inhibitory neurotransmission in mouse colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 1 (January 2004): G110—G117. http://dx.doi.org/10.1152/ajpgi.00148.2003.
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The effects of cannabinoid receptor agonists and antagonists on smooth muscle resting membrane potentials and on membrane potentials following electrical neuronal stimulation in a myenteric neuron/smooth muscle preparation of wild-type and cannabinoid receptor type 1 (CB1)-deficient mice were investigated in vitro. Double staining for CB1 and nitric oxide synthase (neuronal) was performed to identify the myenteric CB1-expressing neurons. Focal electrical stimulation of the myenteric plexus induced a fast (f) excitatory junction potential (EJP) followed by a fast and a slow (s) inhibitory junction potential (IJP). Treatment of wild-type mice with the endogenous CB1 receptor agonist anandamide reduced EJP while not affecting fIJP and sIJP. EJP was significantly higher in CB1-deficient mice than in wild-type littermate controls, and anandamide induced no effects in CB1-deficient mice. N-arachidonoyl ethanolamide (anandamide), R-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3,-de]- 1,4-benzoxazin-6-yl]-1-naphtalenylmethanone, a synthetic CB1 receptor agonist, nearly abolished EJP and significantly reduced the fIJP in wild-type mice. N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole-caroxamide (SR141716A), a CB1-specific receptor antagonist, was able to reverse the agonist effects induced in wild-type mice. SR141716A, when given alone, significantly increased EJP in wild-type mice without affecting IJP in wild-type and EJP in CB1-deficient mice. Interestingly, SR141716A reduced fIJP in CB1-deficient mice. In the mouse colon, nitrergic myenteric neurons do not express CB1, implying that CB1 is expressed in cholinergic neurons, which is in line with the functional data. Finally, excitatory and inhibitory neurotransmission in the mouse colon is modulated by activation of CB1 receptors. The significant increase in EJP in CB1-deficient mice strongly suggests a physiological involvement of CB1 in excitatory cholinergic neurotransmission.
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Wang, L., V. Martínez, H. Kimura, and Y. Taché. "5-Hydroxytryptophan activates colonic myenteric neurons and propulsive motor function through 5-HT4 receptors in conscious mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 1 (January 2007): G419—G428. http://dx.doi.org/10.1152/ajpgi.00289.2006.
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Serotonin [5-hydroxytryptamine (5-HT)] acts as a modulator of colonic motility and secretion. We characterized the action of the 5-HT precursor 5-hydroxytryptophan (5-HTP) on colonic myenteric neurons and propulsive motor activity in conscious mice. Fos immunoreactivity (IR), used as a marker of neuronal activation, was monitored in longitudinal muscle/myenteric plexus whole mount preparations of the distal colon 90 min after an intraperitoneal injection of 5-HTP. Double staining of Fos IR with peripheral choline acetyltransferase (pChAT) IR or NADPH-diaphorase activity was performed. The injection of 5-HTP (0.5, 1, 5, or 10 mg/kg ip) increased fecal pellet output and fluid content in a dose-related manner, with a peak response observed within the first 15 min postinjection. 5-HTP (0.5–10 mg/kg) dose dependently increased Fos expression in myenteric neurons, with a maximal response of 9.9 ± 1.0 cells/ganglion [ P < 0.05 vs. vehicle-treated mice (2.3 ± 0.6 cells/ganglion)]. There was a positive correlation between Fos expression and fecal output. Of Fos-positive ganglionic cells, 40 ± 4% were also pChAT positive and 21 ± 5% were NADPH-diaphorase positive in response to 5-HTP, respectively. 5-HTP-induced defecation and Fos expression were completely prevented by pretreatment with the selective 5-HT4 antagonist RS-39604. These results show that 5-HTP injected peripherally increases Fos expression in different populations of cholinergic and nitrergic myenteric neurons in the distal colon and stimulates propulsive colonic motor function through 5-HT4 receptors in conscious mice. These findings suggest an important role of activation of colonic myenteric neurons in the 5-HT4 receptor-mediated colonic propulsive motor response.
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Green, Christina L., Winnie Ho, Keith A. Sharkey, and Derek M. McKay. "Dextran sodium sulfate-induced colitis reveals nicotinic modulation of ion transport via iNOS-derived NO." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 3 (September 2004): G706—G714. http://dx.doi.org/10.1152/ajpgi.00076.2004.
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In normal colon, ACh elicits a luminally directed Cl− efflux from enterocytes via activation of muscarinic receptors. In contrast, in the murine model of dextran sodium sulfate (DSS)-induced colitis, an inhibitory cholinergic ion transport event due to nicotinic receptor activation has been identified. The absence of nicotinic receptors on enteric epithelia and the ability of nitric oxide (NO) to modulate ion transport led us to hypothesize that NO mediated the cholinergic nicotinic receptor-induced changes in ion transport. Midportions of colon from control and DSS-treated mice were examined for inducible NO synthase (iNOS) expression by RT-PCR and immunofluorescence or mounted in Ussing chambers for assessment of cholinergic-evoked changes in ion transport (i.e., short-circuit current) with or without pretreatment with pharmacological inhibitors of NO production. iNOS mRNA and protein levels were increased throughout the tissue from DSS-treated mice and, notably, in the myenteric plexus, where the majority of iNOS immunoreactivity colocalized with the enteric glial cell marker glial fibrillary acidic protein. The drop in short-circuit current evoked by the cholinomimetic carbachol in tissue from DSS-treated mice was prevented by selective inhibitors of iNOS activity { N6-(1-iminoethyl)-lysine HCl and N-[3-(aminomethyl)benzyl]acetamidine} or an NO scavenger [2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide] or by removal of the myenteric plexus. Thus, in this model of colitis, a “switch” occurs from muscarinic to nicotinic receptor-dominated control of cholinergic ion transport. The data indicate a novel pathway involving activation of nicotinic receptors on myenteric neurons, resulting in release of NO from neurons or enteric glia and, ultimately, a dampening of stimulated epithelial Cl− secretion that would reduce secretory diarrhea.
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Araújo, Eduardo José de Almeida, Débora de Mello Gonçales Sant'Ana, Sônia Lucy Molinari, and Marcílio Hubner de Miranda Neto. "Regional differences in the number and type of myenteric neurons in the descending colon of rats." Arquivos de Neuro-Psiquiatria 61, no. 2A (June 2003): 220–25. http://dx.doi.org/10.1590/s0004-282x2003000200011.
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The purpose of this study was to analyze the neuronal density of the myenteric plexus of the intermediate and antimesocolic regions of the descending colon of rats. Whole-mounts were stained with three different techniques of neuronal evidenciation. Through counts of the number of neurons in an area of 6.64 mm² under light microscopy, we found 1,271 ± 227.54 neurons with Giemsa in the intermediate region and 1,234 ± 225.92 neurons in the antimesocolic region; with the NADH-diaphorase technique we found 530 ± 92.97 neurons in the intermediate region and 539 ± 146.72 neurons in the antimesocolic region; and through the NADPH-diaphorase histochemistry, we found 417 ± 34.42 neurons in the intermediate region and 547 ± 84.01 neurons in the antimesocolic region. We conclude that there is a variation in the density of NADPH-diaphorase positive neurons in the intestinal circumference; that the NADH-diaphorase positive neuronal subpopulation represented 42.7% of that stained with Giemsa; and that the NADPH-diaphorase positive neurons represented 37.8% of the whole myenteric population.
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Capetandes, Anthony, Jerry Di Salvo, John J. Ronan, and Kenneth A. Thomas. "Acidic Fibroblast Growth Factor is Present in the Enteric Nervous System of the Large Intestine." Journal of Histochemistry & Cytochemistry 48, no. 3 (March 2000): 407–13. http://dx.doi.org/10.1177/002215540004800310.
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Acidic fibroblast growth factor (aFGF) is a heparin binding protein that displays pleiotropic activity. The purpose of this study was to document the presence of the translated aFGF product, its mRNA, and its location in the colon. mRNA was extracted from bovine large intestine and reverse transcribed to cDNA. Nested-primer PCR was used to determine the presence of mRNA using primers homologous to the previously published bovine aFGF cDNA. Purification of translated aFGF was performed using an established HPLC protocol. Western blot analysis of the HPLC fractions was performed using two epitopeindependent antibodies against aFGF. Immunohistochemistry employed these antibodies to determine the locus of aFGF expression. The nested-primer PCR product of predicted size was homologous to the published bovine aFGF mRNA sequence, as determined by DNA sequencing. Intestinal aFGF had a mass similar to bovine aFGF isolated from other tissues, and immunocrossreacted with two peptide-based, epitope-independent anti-aFGF antisera on Western blotting. Immunohistochemical analysis of large intestine using these two independent antisera localized aFGF within the myenteric plexus. These data demonstrate that aFGF is present within the myenteric plexus of the enteric nervous system.
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Grider, J. R., A. Arimura, and G. M. Makhlouf. "Role of somatostatin neurons in intestinal peristalsis: facilitatory interneurons in descending pathways." American Journal of Physiology-Gastrointestinal and Liver Physiology 253, no. 4 (October 1, 1987): G434—G438. http://dx.doi.org/10.1152/ajpgi.1987.253.4.g434.
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The role of somatostatin neurons in the regulation of peristalsis was examined in segments of rat colon that permit separate characterization of the ascending contraction and descending relaxation components of the peristaltic reflex. Release of somatostatin and vasoactive intestinal peptide (VIP) increased significantly only during descending relaxation. Preincubation of the segment with somatostatin antiserum (final concentration 1:40) decreased VIP release and descending relaxation. Addition of somatostatin (1 nM to 1 microM) augmented VIP release and descending relaxation in a concentration-dependent manner. Together the results implied that the increase in somatostatin release was coupled to, and responsible for, the increase in VIP release, which in turn was responsible for descending relaxation. The results are consistent with the topography of myenteric VIP neurons (which project into circular muscle) and somatostatin neurons (which project caudad within the plexus) and the pharmacological properties of the two peptides. Somatostatin antiserum had no effect on basal VIP release or ascending contraction, indicating that somatostatin neurons were not involved in the regulation of ascending contraction. The study suggests that somatostatin neurons of the myenteric plexus act as facilitatory interneurons in descending pathways.