Journal articles: 'Duodenum – Innervation'

1

Li, Cuiping, Yaohui Zhu, Mohan Shenoy, Reetesh Pai, Liansheng Liu, and Pankaj Jay Pasricha. "Anatomical and functional characterization of a duodeno-pancreatic neural reflex that can induce acute pancreatitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 5 (March 1, 2013): G490—G500. http://dx.doi.org/10.1152/ajpgi.00012.2012.

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Neural cross talk between visceral organs may play a role in mediating inflammation and pain remote from the site of the insult. We hypothesized such a cross talk exists between the duodenum and pancreas, and further it induces pancreatitis in response to intraduodenal toxins. A dichotomous spinal innervation serving both the duodenum and pancreas was examined, and splanchnic nerve responses to mechanical stimulation of these organs were detected. This pathway was then excited on the duodenal side by exposure to ethanol followed by luminal mustard oil to activate transient receptor potential subfamily A, member 1 (TRPA1). Ninety minutes later, pancreatic inflammation was examined. Ablation of duodenal afferents by resiniferatoxin (RTX) or blocking TRPA1 by Chembridge (CHEM)-5861528 was used to further investigate the duodeno-pancreatic neural reflex via TRPA1. ∼40% of dorsal root ganglia (DRG) from the spinal cord originated from both duodenum and pancreas via dichotomous peripheral branches; ∼50% splanchnic nerve single units responded to mechanical stimulation of both organs. Ethanol sensitized TRPA1 currents in cultured DRG neurons. Pancreatic edema and myeloperoxidase activity significantly increased after intraduodenal ethanol followed by mustard oil (but not capsaicin) but significantly decreased after ablation of duodenal afferents by using RTX or blocking TRPA1 by CHEM-5861528. We found the existence of a neural cross talk between the duodenum and pancreas that can promote acute pancreatitis in response to intraduodenal chemicals. It also proves a previously unexamined mechanism by which alcohol can induce pancreatitis, which is novel both in terms of the site (duodenum), process (neurogenic), and receptor (TRPA1).

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Zhang, Xueguo, William E. Renehan, and Ronald Fogel. "Vagal innervation of the rat duodenum." Journal of the Autonomic Nervous System 79, no. 1 (February 2000): 8–18. http://dx.doi.org/10.1016/s0165-1838(99)00093-4.

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Raybould, H. E., and H. H. Holzer. "Duodenal acid-induced inhibition of gastric motility and emptying in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 3 (September 1, 1993): G540—G546. http://dx.doi.org/10.1152/ajpgi.1993.265.3.g540.

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The mechanism by which acid in the duodenum inhibits proximal gastric motor function and delays emptying was investigated in urethan-anesthetized and awake rats. Gastric motility inhibited by duodenal acid (0.2 N HCl) in urethan-anesthetized rats was attenuated by 68 and 54%, respectively, by functional ablation of the vagal or spinal sensory innervation with capsaicin. 5-Hydroxytryptamine3 receptor blockade with zacopride (0.2 mg/kg ip) or cholecystokinin (CCK)-A-type receptor blockade with MK-329 (1 mg/kg ip) had no effect on the motility response to acid. In awake rats with chronically implanted gastric and duodenal cannulas, perfusion of the duodenum with acid (0.1 and 0.2 N HCl) inhibited gastric emptying of a nonnutrient liquid (38 and 59%, respectively). Blockade of CCK-A-type receptors reduced by 30% inhibition of gastric emptying induced by 0.1 N HCl. However, functional ablation of the vagal or spinal sensory innervation, 5-hydroxytryptamine3 receptor blockade, or immunoneutralization of secretin by systemic administration of a polyclonal antibody (no. 7842, 1 ml ip) had no effect on acid-induced (0.1 N HCl) inhibition of gastric emptying. Perfusion of the duodenum with 0.2 N HCl but not 0.1 N HCl inhibited proximal gastric motility in awake rats. These results suggest that 1) a duodenal acid load inhibits gastric emptying in part by a mechanism involving CCK and 2) decreased proximal gastric motility plays a minor role in inhibition of gastric emptying in response to acid.

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Holzer, H. H., C. M. Turkelson, T. E. Solomon, and H. E. Raybould. "Intestinal lipid inhibits gastric emptying via CCK and a vagal capsaicin-sensitive afferent pathway in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 4 (October 1, 1994): G625—G629. http://dx.doi.org/10.1152/ajpgi.1994.267.4.g625.

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The mechanism by which lipid in the duodenum inhibits gastric emptying was investigated in awake rats fitted with chronic gastric and duodenal cannulas. Perfusion of the duodenum with lipid (Intralipid, 5 and 10%; total amount 50 and 100 mg) caused a significant inhibition (26 and 78%, respectively) of gastric emptying of a nonnutrient liquid (0.9% saline). Functional ablation of the capsaicin-sensitive vagal, but not the spinal, sensory innervation to the upper gastrointestinal tract significantly attenuated by 57% lipid-induced inhibition of gastric emptying. In intact rats, administration of a specific cholecystokinin (CCK)-A receptor antagonist, devazepide, significantly attenuated by 66% the response to lipid. Administration of devazepide in perivagal capsaicin-treated rats did not further reduce the response to lipid. These results suggest that lipid in the duodenum inhibits gastric emptying via a mechanism involving an action of CCK at type A receptors and capsaicin-sensitive vagal afferents.

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Berthoud, H. R., N. R. Carlson, and T. L. Powley. "Topography of efferent vagal innervation of the rat gastrointestinal tract." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 1 (January 1, 1991): R200—R207. http://dx.doi.org/10.1152/ajpregu.1991.260.1.r200.

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The gastrointestinal territories innervated by the gastric, celiac, and hepatic abdominal vagi were identified in rats with selective branch vagotomies by means of 1) anterograde tracing with the carbocyanine dye DiI injected into the dorsal motor nucleus and 2) measurement of cervical vagal stimulation-induced motility responses throughout the gut axis. Presence of DiI-labeled vagal terminals in the myenteric plexus and evoked motility responses were well correlated across the sampled gastrointestinal (GI) sites. In animals with only the two gastric branches intact, the entire stomach and the most proximal duodenum showed significant motility responses and were densely innervated, having DiI-labeled vagal terminals in almost every ganglion. The hepatic branch was found to primarily innervate the duodenum, with minor projections to the distal antral stomach and the intestines. The two celiac branches were found to almost exclusively innervate the jejunum, ileum, cecum and entire colon, and, together with the other vagal branches, the duodenum. Therefore, while there is some degree of specific innervation by the abdominal vagal branches of the oral-to-anal gut axis, which could be called "viscerotopic," the considerably overlapping innervation of the duodenum does not satisfy a viscerotopy criterion and needs further functional analysis.

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6

Behrns, K. E., M. G. Sarr, R. B. Hanson, and A. R. Zinsmeister. "Neural control of canine small intestinal motility during nonnutrient infusion." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 3 (September 1, 1996): G423—G432. http://dx.doi.org/10.1152/ajpgi.1996.271.3.g423.

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Our aim was to determine the effect of in situ neural isolation of the jejunoileum (extrinsic denervation and disruption of enteric neural continuity with the duodenum) on the spread of single pressure waves (SPW) and clustered contractions (CC) in response to increasing rates of isolated duodenal and jejunoileal nonnutrient infusions. Ten dogs were prepared with duodenal and jejunal infusion and manometry catheters and a diverting proximal jejunal cannula. Five of the dogs also underwent in situ neural isolation of the entire jejuno- ileum A noncaloric solution was infused at 0-15 ml/min into proximal duodenum or jejunum while manometric data were collected. Alterations in direction, distance, and velocity of spread of SPW and CC with increasing rates of intestinal infusion were analyzed by linear regression of responses to increasing infusion rates. Neural isolation of the jejunoileum did not markedly alter characteristics of duodenal or jejunal SPW or CC under conditions of no intestinal infusion. After neural isolation of jejunoileum, increasing rates of jejunal infusion decreased both the proportion and distance of antegrade spread of SPW in duodenum. These findings suggest that extrinsic innervation to the jejunoileum and enteric neural continuity with the duodenum do not regulate jejunal SPW or CC. Increasing rates of nonnutrient intestinal infusions do not alter local motor patterns in the innervated or neurally isolated jejunum, but after neural isolation of the jejunoileum, these infusions do alter characteristics of duodenal SPW by mechanisms independent of neural pathways.

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7

Holle, G. E., D. Hahn, and W. Forth. "Innervation of pylorus in control of motility and gastric emptying." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 2 (August 1, 1992): G161—G168. http://dx.doi.org/10.1152/ajpgi.1992.263.2.g161.

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The motility index (MI) and contractile frequency were determined for the gastric antrum, pylorus, and duodenum during digestive and interdigestive states in eight dogs before and after resection of the ramus pyloricus nervi vagi (NR) and after selective proximal vagotomy (SPV) subsequent to NR. Neither NR nor subsequent SPV altered the migrating motor complex in the interdigestive state. In the digestive state, NR decreased the MI in the antrum, pylorus, and duodenum. The MI did not further change after SPV subsequent to NR. The cholecystokinin antagonist L364,718 decreased MI in the antrum, pylorus, and duodenum. After NR, L364,718 caused a further reduction in the MI during administration. Gastric emptying was accelerated after NR. SPV subsequent to NR increased gastric emptying further. L364,718, in the absence of NR, accelerated gastric emptying but only during the initial period of emptying. After NR, L364,718 also decreased the time required for emptying of 50 and 100% of the meal. After SPV subsequent to NR, no additional acceleration of emptying occurred.

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8

Khurana, Ramesh K., and J. M. Petras. "Sensory innervation of the canine esophagus, stomach, and duodenum." American Journal of Anatomy 192, no. 3 (November 1991): 293–306. http://dx.doi.org/10.1002/aja.1001920309.

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9

Tomaszewska, O., and J. Kaleczyc. "The distribution and chemical coding of neurons supplying the sphincter of Oddi in mammals." Polish Journal of Veterinary Sciences 16, no. 4 (December 1, 2013): 787–96. http://dx.doi.org/10.2478/pjvs-2013-0113.

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Abstract The major duodenal papilla (papilla of Vater) is an important structure associated with the biliary tract and, in some species, the pancreas. It usually represents a slight elevation on the intestinal mucosa where the dilated junction (ampulla of Vater) of the commmon bile duct and pancreatic duct enters the duodenum. The ampulla is surrounded by a specifically arranged muscle structure called the sphincter of Oddi (SO) which controls the flow of bile and pancreatic fluid. The function of the sphincter is regulated by a complex system that involves many hormonal and neural factors. The literature in the field contains detailed data on the morphology of the SO in a number of mammalian species. However, the comprehensive information about the anatomy and neurochemistry of the innervation of this structure is very limited. The present review article summarizes the current knowledge on the innervation of the SO in mammals. Special emphasis has been put on the localization and chemical coding of neurons contributing to this nerve supply.

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10

Stojanovic, Marija, Lj Scepanovic, D. Mitrovic, V. Scepanovic, T. Stojanovic, M. Stojkovic, S. Ilic, and D. Djuric. "Rat duodenal motility in vitro: Prokinetic effects of DL-homocysteine thiolactone and modulation of nitric oxide mediated inhibition." Archives of Biological Sciences 65, no. 4 (2013): 1323–30. http://dx.doi.org/10.2298/abs1304323s.

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Homocysteine is a significant but modifiable risk factor for vascular diseases. As gastrointestinal smooth musculature is similar to blood vessel muscles, we investigated how elevated homocysteine levels affect nitric oxide-mediated neurotransmission in the gut. There is accumulated evidence that a dysfunction of NO neurons in the myenteric plexus may cause various diseases in the gastrointestinal tract such as achalasia, diabetic gastroparesis and infantile hypertrophic pyloric stenosis. In the present study, we aimed to assess the effects of homocysteine on NO-mediated responses in vitro, and to examine the effects of DL-homocysteine thiolactone on the spontaneous motility of rat duodenum and nitrergic neurotransmission. DL-homocysteine thiolactone concentration of 10 ?mol/L leads to the immediate increase in tone, amplitude and frequency of spontaneous movements in isolated rat duodenum. L-NAME (30 ?mol/L) leads to an increase in basal tone, amplitude and frequency of spontaneous contractions. The relaxations induced by EFS were significantly reduced in duodenal segments incubated in DL-homocysteine thiolactone compared with the control group. EFS-induced relaxations were inhibited by L-NAME in both experimental and control groups. These results suggest that a high level of homocysteine causes an important impairment of non-adrenergic non-cholinergic innervation of the rat duodenum.

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11

IINO, Satoshi. "Muscular Innervation of the Proximal Duodenum of the Guinea Pig." Archives of Histology and Cytology 63, no. 4 (2000): 327–43. http://dx.doi.org/10.1679/aohc.63.327.

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12

Bendeck, M. P., and R. P. E. Reynolds. "Gastric and duodenal motility in the cat: the role of central innervation assessed by transient vagal blockade." Canadian Journal of Physiology and Pharmacology 64, no. 6 (June 1, 1986): 712–16. http://dx.doi.org/10.1139/y86-119.

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Experiments were performed on four cats to characterize fasting gastric and small bowel motility and to assess the role of extrinsic vagal innervation in the control of that motor activity. A multilumen manometry tube was positioned to record pressure changes from the proximal small bowel and stomach. Transient vagal nerve blockade was accomplished by cooling the cervical vagosympathetic nerve trunks, previously isolated in skin loops on each side of the neck. Two characteristic patterns of basal activity were documented in the stomach: (i) regular phasic contractions of variable amplitude in the body of the stomach; and (ii) infrequent, irregular contractions of high amplitude in the distal antrum. In the duodenum, two predominant activity patterns were noted: (i) periods of continuous irregular activity; and (ii) irregular clusters of contractions separated by quiescent intervals. No typical migrating motor complex activity was seen in the basal gastric or small bowel recordings. Bilateral vagal blockade did not consistently change the general pattern of gastric or small bowel activity, but did appear to reduce gastric contractile activity, as measured by motility indices. We conclude that extrinsic vagal innervation does not play a major role in the control of fasting feline gastric and duodenal motility.

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13

Takio Kitazawa, Hidenari Furuhashi, Kenji Umezawa, Masaki Morioka, Kyosuke Temma, and Horoshi Kondo. "Is there functional cholinergic innervation in the frog duodenum (Rana catesbiana)?" Comparative Biochemistry and Physiology Part C: Comparative Pharmacology 85, no. 2 (January 1986): 275–82. http://dx.doi.org/10.1016/0742-8413(86)90194-5.

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14

Behrns, Kevin E., Michael G. Sarr, Russell B. Hanson, and Alan R. Zinsmeister. "Canine small bowel motor patterns and contractions are not neurally regulated during enteric nutrient infusion." American Journal of Physiology-Gastrointestinal and Liver Physiology 274, no. 5 (May 1, 1998): G912—G922. http://dx.doi.org/10.1152/ajpgi.1998.274.5.g912.

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The aims of this study were to determine the effects of duodenal and jejunoileal nutrient infusions on small intestinal motor patterns and intestinal contractions in neurally intact and neurally isolated small bowel. Fifteen dogs were prepared with duodenal and jejunal infusion and manometry catheters and a diverting jejunal cannula. Ten of the dogs underwent in situ neural isolation of the jejunoileum. A mixed nutrient meal (0.5 kcal/ml) was infused into the duodenum or jejunum at 3 ml/min for 5 h. Control experiments involved infusion of a balanced salt solution. Manometric data collected on-line to a microcomputer were analyzed for direction, distance, and velocity of spread of single pressure waves (SPW) and clustered contractions. Isolated duodenal and jejunoileal nutrient infusions inhibited the fasting motor pattern in neurally intact and neurally isolated small bowel. Motor activity (motility index) increased slightly during nutrient infusion within groups, but there were few differences between groups. Neither neural isolation nor nutrient infusion had a consistent effect on spread of SPW or migration of clustered contractions. Isolated duodenal and jejunoileal nutrient infusions in the dog inhibit fasting motor patterns and increase motor activity slightly but have little effect on characteristics of individual and clustered contractions. Extrinsic innervation to the jejunoileum or intrinsic neural continuity of the jejunum with the duodenum had little effect on single or grouped contractions. Although the changes in motor activity demonstrated in this study appear small, alterations in intestinal transit and absorption may still occur and may be of importance physiologically.

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Smith, V. C., N. Dhatt, and A. MJ Buchan. "The innervation of the human antro-pyloric region: Organization and composition." Canadian Journal of Physiology and Pharmacology 79, no. 11 (November 1, 2001): 905–18. http://dx.doi.org/10.1139/y01-075.

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Although the composition of the gastric innervation has been determined in animal models, relatively little known about the innervation of the human antro-pyloric region. We used immunocytochemical techniques to establish the localization and co-expression of neuropeptides and nitric oxide in the human antrum and upper duodenum. Our results demonstrate the existence of a clearly defined submucosal plexus in the antral region that is absent in rats and guinea pigs. The abundant innervation of the lamina propria contains 3 major nerve populations: VIP- and NOS-, SP- and CGRP-, and GRP-immunoreactive. For the first time, NOS-containing nerve fibers were observed throughout the length of the antral glands. Within the antrum somatostatin was confined to endocrine cells, however, at the pyloric sphincter both enteric plexi contained immunoreactive neurons and nerve fibres. Within the pyloric sphincter CGRP- and SP-immunoreactive fibres were significantly increased, correlating with the presence of large ganglia in the submucosal plexus. In conclusion, the organization and composition of the innervation of human antro-pylorus differed substantially from that reported in other mammals. The presence of an abundant mucosal innervation paralled by a well-defined submucosal plexus indicates that the functional regulation of the gastricpyloric region will be distinct from that of smaller animal models.Key words: gastric innervation, pyloric sphincter, neuropeptides, nitric oxide, somatostatin.

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Struller, Florian, Frank-Jürgen Weinreich, Philipp Horvath, Marios-Konstantinos Kokkalis, Stefan Beckert, Alfred Königsrainer, and Marc A. Reymond. "Peritoneal innervation: embryology and functional anatomy." Pleura and Peritoneum 2, no. 4 (December 20, 2017): 153–61. http://dx.doi.org/10.1515/pp-2017-0024.

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AbstractThe parietal peritoneum (PP) is innervated by somatic and visceral afferent nerves. PP receives sensitive branches from the lower intercostal nerves and from the upper lumbar nerves. Microscopically, a dense network of unmyelinated and myelinated nerve fibers can be found all over the PP. The unmyelinated fibers are thin and are ending just underneath the PP. The myelinated fibers can penetrate the PP to reach the peritoneal cavity, where they lose their myelin sheath and are exposed to somatic and nociceptive stimuli. PP is sensitive to pain, pressure, touch, friction, cutting and temperature. Noxious stimuli are perceived as a localized, sharp pain. The visceral peritoneum (VP) itself is not innervated, but the sub-mesothelial tissue is innervated by the autonomous nerve system. In contrast to the PP, the visceral submesothelium also receives fibers from the vagal nerve, in addition to the spinal nerves. VP responds primarily to traction and pressure; not to cutting, burning or electrostimulation. Painful stimuli of the VP are poorly localized and dull. Pain in a foregut structure (stomach, duodenum or biliary tract) is referred to the epigastric region, pain in a midgut structure (appendix, jejunum, or ileum) to the periumbilical area and pain from a hindgut source (distal colon or rectum) is referred to the lower abdomen or suprapubic region. Peritoneal adhesions can contain nerve endings. Neurotransmitters are acetylcholine, VIP, serotonin, NO, encephalins, CGRP and substance P. Chronic peritoneal pain can be exacerbated by neurogenic inflammation, e.g. by endometriosis.

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Padbury, R. T. A., R. A. Baker, J. P. Messenger, J. Toouli, and J. B. Furness. "Structure and Innervation of the Extrahepatic Biliary System in the Australian Possum, Trichosurus Vulpecula." HPB Surgery 7, no. 2 (January 1, 1993): 125–40. http://dx.doi.org/10.1155/1993/72946.

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The morphology, microanatomy and innervation of the biliary tree of the Australian possum, Trichosurus vulpecula, was examined. The gross morphology of the gallbladder, hepatic and cystic ducts, and the course of the common bile duct, conforms to those of other species. The sphincter of Oddi has an extraduodenal segment that extends 15mm from the duodenal wall; within this segment the pancreatic and common bile ducts are ensheathed together by sphincter muscle. Their lumens unite to form a common channel within the terminal intraduodenal segment.Nerve cell bodies of the gallbladder were found in an inter-connecting network of ganglia that were located in the serosa, muscularis and mucosa. Nerve fibres innervated the muscle, arterioles and the mucosa. Few ganglia were found along the supra sphincteric portion of the common bile duct. Nerve trunks followed the duct and a dense nerve fibre plexus was found in the mucosa. In the sphincter most ganglia were located in two plexuses, the first between the layers of the external sphincter muscle, which was continuous with the external muscle of the duodenum, and the second was associated with the internal sphincter muscle. Nerve fibres were numerous in the sphincter muscle, and were also found in the subepithelial and periglandular plexuses of both the pancreatic and common bile ducts.

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Holzer, H. H., and H. E. Raybould. "Vagal and splanchnic sensory pathways mediate inhibition of gastric motility induced by duodenal distension." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 4 (April 1, 1992): G603—G608. http://dx.doi.org/10.1152/ajpgi.1992.262.4.g603.

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Afferent pathways mediating gastric corpus relaxation after duodenal distension were studied in urethan-anesthetized rats in which the sensory neurotoxin capsaicin (1%) or its vehicle was applied directly to the cervical vagus nerve trunks or the celiac-superior mesenteric ganglia 10-20 days before experiments. Distension (0.05-0.5 ml) of a closed loop of proximal duodenum decreased gastric intraluminal pressure. Perineural capsaicin treatment to the vagus nerves decreased by 73 and 80% the response to low volumes of distension (0.05 and 0.1 ml). Perineural capsaicin treatment of the celiac-superior mesenteric ganglia significantly attenuated by 46-88% the response to all volumes of distension. Bilateral cervical vagotomy or ganglionectomy reduced the response to all volumes of duodenal distension and, in combination, abolished the response. It is concluded that the decrease in gastric corpus motility after duodenal distension is dependent on the extrinsic innervation to the upper gastrointestinal tract and is mediated by both vagal and spinal capsaicin-sensitive afferents. Capsaicin-sensitive vagal afferents mediate responses to low volumes of distension that may be physiological. Capsaicin-sensitive spinal afferents mediate the gastric response to higher volumes of distension and may be involved in mediating visceral and somatic responses to pathophysiological intestinal obstruction.

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Chung, S. A., O. Rotstein, G. R. Greenberg, and N. E. Diamant. "Mechanisms coordinating gastric and small intestinal MMC: role of extrinsic innervation rather than motilin." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 5 (November 1, 1994): G800—G809. http://dx.doi.org/10.1152/ajpgi.1994.267.5.g800.

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We have investigated the role of vagal and efferent adrenergic innervation coordinating the gastric and small intestinal migrating motor complexes (MMCs) after removal of the pylorus, duodenum, and upper jejunum in three dogs. The cervical vagus nerves were previously isolated in bilateral skin loops to permit reversible cooling blockade of the vagi. Pharmacological alpha- and beta-receptor blockade was accomplished by bolus intravenous injection of phentolamine and propranolol followed by intravenous infusion of the combined drugs. Gastric and upper jejunal MMC-like activity was initially absent after bowel resection but reappeared after 1-4 mo with the gastric and jejunal MMC-like activities coordinated as if the jejunum were the duodenum. Motilin peaks were absent. All gastric contractions were abolished by vagal blockade. Pharmacological adrenergic blockade immediately induced an intense burst of contractile and electrical activity in the stomach, which propagated to the distal ileum. This phase III-like burst was followed by ongoing intermittent bursts of contractile and electrical activity in the stomach and small intestine, lasting throughout the blockade, without further MMC-like activity. Vagal cooling blockade in combination with adrenergic blockade did not restore gastric MMC-like activity but abolished or decreased the number of gastric contractions, with the reappearance of the small intestinal MMC. Atropine boluses abolished all control and adrenergic blockade-induced stomach and small intestinal contractile and electrical activity. In conclusion, after duodenectomy, the gastric MMC-like activity that is reestablished and is coordinated with the small intestinal MMC is vagally dependent and cholinergic, but its cyclical nature requires adrenergic efferent pathways. Under these circumstances, coordination of the gastric and jejunal MMCs appears to require extrinsic innervation.

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Mulè, F., A. Geraci, R. Serio, and A. Postorino. "On the peptidergic hypothesis for non-adrenergic non-cholinergic innervation in the rat duodenum." Journal of Autonomic Pharmacology 12, no. 2 (April 1992): 81–88. http://dx.doi.org/10.1111/j.1474-8673.1992.tb00365.x.

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Höckerfelt, Ulf, Lars Franzén, and Sture Forsgren. "Substance P (NK1) receptor in relation to substance P innervation in rat duodenum after irradiation." Regulatory Peptides 98, no. 3 (April 2001): 115–26. http://dx.doi.org/10.1016/s0167-0115(00)00233-0.

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Fox, Edward A., Robert J. Phillips, Fred A. Martinson, Elizabeth A. Baronowsky, and Terry L. Powley. "Vagal afferent innervation of smooth muscle in the stomach and duodenum of the mouse: Morphology and topography." Journal of Comparative Neurology 428, no. 3 (2000): 558–76. http://dx.doi.org/10.1002/1096-9861(20001218)428:3<558::aid-cne11>3.0.co;2-m.

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Porcher, Christophe, Yvon Julé, and Monique Henry. "A Qualitative and Quantitative Study on the Enkephalinergic Innervation of the Pig Gastrointestinal Tract." Journal of Histochemistry & Cytochemistry 48, no. 3 (March 2000): 333–43. http://dx.doi.org/10.1177/002215540004800303.

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Enkephalins are involved in neural control of digestive functions such as motility, secretion, and absorption. To better understand their role in pigs, we analyzed the qualitative and quantitative distribution of enkephalin immunoreactivity (ENK-IR) in components of the intestinal wall from the esophagus to the anal sphincter. Immunohistochemical labelings were analyzed using conventional fluorescence and confocal microscopy. ENK-IR was compared with the synaptophysin immunoreactivity (SYN-IR). The results show that maximal ENK-IR levels in the entire digestive tract are reached in the myenteric plexuses and, to a lesser extent, in the external submucous plexus and the circular muscle layer. In the longitudinal muscle layer, ENK-IR was present in the esophagus, stomach, rectum, and anal sphincter, whereas it was absent from the duodenum to the distal colon. In the ENK-IR plexuses and muscle layers, more than 60% of the nerve fibers identified by SYN-IR expressed ENK-IR. No ENK-IR was observed in the internal submucous plexus and the mucosa; the latter was found to contain ENK-IR endocrine cells. These results strongly suggest that, in pigs, enkephalins play a major role in the regulatory mechanisms that underlie the neural control of digestive motility.

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Spencer, M. P., M. G. Sarr, N. J. Soper, and N. S. Hakim. "Jejunal regulation of gastric motility patterns: effect of extrinsic neural continuity to stomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 258, no. 1 (January 1, 1990): G32—G37. http://dx.doi.org/10.1152/ajpgi.1990.258.1.g32.

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This study was designed to determine the role of extrinsic gastric innervation in mediating the inhibitory effects of jejunal infusion of mixed nutrients on canine interdigestive gastric motility patterns. Four dogs underwent transection of all extrinsic and intrinsic neural continuity to the stomach except for careful preservation of vagal innervation (stage 1). Antral manometry catheters, antral electrodes, intestinal electrodes, and a jejunal infusion catheter were placed. After a 2-wk recovery, stage 1 studies of myoelectric and contractile activity of the stomach and small bowel during fasting were recorded on four occasions during infusion of isomolar solutions of either nonnutrient NaCl (150 mM) or mixed nutrients (50% Meritene solution) into the jejunum at 2.9 ml/min for 6 h. Identical studies (stage 2) were repeated after completion of extrinsic denervation of the stomach by supradiaphragmatic vagotomy. In stage 1 studies, jejunal nutrients (83 kcal/h) inhibited the characteristic interdigestive cyclic motility patterns in the stomach and duodenum for greater than or equal to 172 min during jejunal infusion of mixed nutrients. After completion of extrinsic denervation (stage 2), jejunal infusion of nutrients had the same effects with inhibition of cyclic motility patterns in the stomach and small intestine. We concluded that inhibition of interdigestive gastric motility patterns by jejunally infused nutrients is mediated by hormonal mechanisms and not by nonvagal or vagal extrinsic neural input to the stomach.

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Zhao, Huan, Leslie K. Sprunger, and Steven M. Simasko. "Expression of transient receptor potential channels and two-pore potassium channels in subtypes of vagal afferent neurons in rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 2 (February 2010): G212—G221. http://dx.doi.org/10.1152/ajpgi.00396.2009.

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Vagal afferent neurons relay important information regarding the control of the gastrointestinal system. However, the ionic mechanisms that underlie vagal activation induced by sensory inputs are not completely understood. We postulate that transient receptor potential (TRP) channels and/or two-pore potassium (K2p) channels are targets for activating vagal afferents. In this study we explored the distribution of these channels in vagal afferents by quantitative PCR after a capsaicin treatment to eliminate capsaicin-sensitive neurons, and by single-cell PCR measurements in vagal afferent neurons cultured after retrograde labeling from the stomach or duodenum. We found that TRPC1/3/5/6, TRPV1-4, TRPM8, TRPA1, TWIK2, TRAAK, TREK1, and TASK1/2 were all present in rat nodose ganglia. Both lesion results and single-cell PCR results suggested that TRPA1 and TRPC1 were preferentially expressed in neurons that were either capsaicin sensitive or TRPV1 positive. Expression of TRPM8 varied dynamically after various manipulations, which perhaps explains the disparate results obtained by different investigators. Last, we also examined ion channel distribution with the A-type CCK receptor (CCK-RA) and found there was a significant preference for neurons that express TRAAK to also express CCK-RA, especially in gut-innervating neurons. These findings, combined with findings from prior studies, demonstrated that background conductances such as TRPC1, TRPA1, and TRAAK are indeed differentially distributed in the nodose ganglia, and not only do they segregate with specific markers, but the degree of overlap is also dependent on the innervation target.

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Holle, G. E., and W. Forth. "Myoelectric activity of small intestine after chemical ablation of myenteric neurons." American Journal of Physiology-Gastrointestinal and Liver Physiology 258, no. 4 (April 1, 1990): G519—G526. http://dx.doi.org/10.1152/ajpgi.1990.258.4.g519.

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Ablation of the myenteric plexus was performed by serosal application of 0.062% benzalkonium chloride (BAC) in the duodenum, proximal and distal jejunum, and ileum. The thickness of muscle layers and the number and sizes of ganglia and neurons of the myenteric plexus were evaluated before and 21-28 days after treatment. Electrodes were implanted on the treated segments and on segments orad and aborad to the treated segment. The electromyogram of each segment was recorded daily for periods of 2-3 h. The number of myenteric neurons in the BAC-treated segment was decreased significantly by 85 to 98% relative to segments removed before BAC application. Significantly, thickening of longitudinal plus circular muscle layers amounted to 113% in the duodenum and 261% in the ileum in the treated segment. No changes were observed in electrical slow-wave frequency in treated segments. Spike activity (percentage of slow waves with spikes) increased in the BAC-treated segment by 92% compared with recording sites orad and aborad to the treated segment and to the small intestine in untreated control animals. We interpreted the increase in spike activity in treated segments to reflect the loss of inhibitory neuronal influence. The hyperplasia and hypertrophy of the longitudinal and circular muscle coat could have resulted from a direct influence of the altered innervation or from work-induced hypertrophy in the treated segment secondary to uncoordinated hyperactivity of the disinhibited musculature.

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Fujimiya, Mineko, Hiroshi Yamamoto, and Atsukazu Kuwahara. "Effect of VIP and PACAP on basal release of serotonin from isolated vascularly and luminally perfused rat duodenum." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 4 (October 1, 1998): G731—G739. http://dx.doi.org/10.1152/ajpgi.1998.275.4.g731.

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The effect of vasoactive intestinal polypeptide (VIP), pituitary adenylate cyclase-activating peptide-38 (PACAP-38), and PACAP-27 on the release of serotonin (5-HT) into the intestinal lumen and the portal circulation was studied by using in vivo isolated vascularly and luminally perfused rat duodenum. 5-HT levels were determined by HPLC. VIP, PACAP-38, and PACAP-27 reduced the luminal release of 5-HT but did not affect the vascular release of 5-HT. The inhibitory effect caused by VIP, PACAP-38, and PACAP-27 was not affected by either atropine, hexamethonium, TTX, or TTX plus ACh, but it was completely antagonized by the nitric oxide (NO) synthase inhibitor NG-nitro-l-arginine (l-NNA). The VIP receptor antagonist VIP-(10—28) blocked the effects of VIP, PACAP-38, and PACAP-27. These results suggest that VIP and PACAP exert a direct inhibitory effect on the luminal release of 5-HT from the enterochromaffin (EC) cells via a common receptor site on the EC cells and that this effect is mediated by NO but not by cholinergic pathways. A single injection of TTX, atropine, or hexamethonium reduced the luminal release of 5-HT, whereas a single injection of VIP-(10—28) stimulated the luminal release of 5-HT and this effect was antagonized by atropine, hexamethonium, or TTX. These results suggest that EC cells may receive the direct innervation of cholinergic neurons as well as VIP and/or PACAP neurons, with the former exerting a tonic stimulatory influence and the latter exerting a tonic inhibitory influence on 5-HT release into the intestinal lumen.

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Dixon, Kimberly D., Fred E. Williams, Raymond L. Wiggins, Jason Pavelka, James Lucente, Larry L. Bellinger, and Dorothy W. Gietzen. "Differential effects of selective vagotomy and tropisetron in aminoprivic feeding." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 3 (September 1, 2000): R997—R1009. http://dx.doi.org/10.1152/ajpregu.2000.279.3.r997.

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Both total subdiaphragmatic vagotomy (TVAGX) and serotonin3 receptor blockade with tropisetron or ondansetron attenuate amino acid-imbalanced diet (Imb) anorexia. Total vagotomy is less effective than tropisetron in reducing Imb-induced anorexia and also blunts the tropisetron effect. With the use of electrocautery at the subdiaphragmatic level of the vagus, we severed the ventral and dorsal trunks as well as the hepatic, ventral gastric, dorsal gastric, celiac, and accessory celiac branches separately or in combination to determine which vagal branches or associated structures may be involved in these responses. Rats were prefed a low-protein diet. On the first experimental day, tropisetron or saline was given intraperitoneally 1 h before presentation of Imb. Cuts including the ventral branch, i.e., TVAGX, ventral vagotomy (above the hepatic branch), and hepatic + gastric vagotomies (but not hepatic branch cuts alone) caused the highest ( P < 0.05) Imb intake on day 1 with or without tropisetron. The responses to tropisetron were not affected significantly. On days 2–8, groups having vagotomies that included the hepatic branch recovered faster than sham-treated animals. Because the hepatic and gastric branches together account for most of the vagal innervation to the proximal duodenum, this area may be important in the initial responses, whereas structures served by the hepatic branch alone apparently act in the later adaptation to Imb.

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Peters, J. H., R. C. Ritter, and S. M. Simasko. "Leptin and CCK selectively activate vagal afferent neurons innervating the stomach and duodenum." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 6 (June 2006): R1544—R1549. http://dx.doi.org/10.1152/ajpregu.00811.2005.

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The hormone leptin and the gut peptide CCK synergistically interact to enhance the process of satiation. Although this interaction may occur at several levels of the neuroaxis, our previous results indicate that leptin can specifically enhance the satiation effect of CCK by acting on subdiaphragmatic vagal afferent neurons. Because of this localized action, we hypothesized that a high proportion of vagal afferent neurons innervating the stomach or duodenum would be responsive to leptin and/or CCK. To test this hypothesis, we measured changes in cytosolic calcium levels induced by leptin and CCK in cultured nodose ganglion neurons labeled with a retrograde neuronal tracer injected into either the stomach or the duodenum. In the neurons labeled from the stomach, CCK activated 74% (39 of 53) compared with only 35% (34 of 97) of nonlableled cells. Of the CCK-responsive neurons 60% (18 of 30) were capsaicin-sensitive. Leptin activated 42% (22 of 53) of the stomach innervating neurons compared with 26% of nonlabeled neurons. All of the leptin-sensitive neurons labeled from the stomach also responded to CCK. In the neurons labeled from the duodenum, CCK activated 71% (20 of 28). Of these CCK-responsive neurons 80% (12 of 15) were capsaicin sensitive. Leptin activated 46% (13 of 28) of these duodenal innervating neurons, of which 89% (8 of 9) were capsaicin-sensitive. Among neurons labeled from the duodenum 43% (12 of 28) were responsive to both leptin and CCK, compared with only 15% (15 of 97) of unlabeled neurons. Our results support the hypothesis that vagal afferent sensitivity to CCK and leptin is concentrated in neurons that innervate the stomach and duodenum. These specific visceral afferent populations are likely to comprise a substrate through which acute leptin/CCK interactions enhance satiation.

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Kurnikova, Irina Alekseevna, Tatiana Evgen'evna Chernyshova, Irina Vladimirovna Gur'eva, and Guzyal' Ilgisovna Kliment'eva. "Clinico-expert diagnostics of gastrointestinal form of diabetic neuropathy." Diabetes mellitus 14, no. 2 (June 15, 2011): 94–97. http://dx.doi.org/10.14341/2072-0351-5644.

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Aim. To estimate dynamics of secretory and motor-evacuational functions of the stomach in patients with type 1 diabetes mellitus and gastrointestinalform of diabetic neuropathy. Materials and methods. 32 patients with DM1 without gastrointestinal pathology allocated to different groups depending on DM duration (gr. 1 lessthan 10 yr, gr. 2 over 10 yr). Vegetative equilibrium was estimated from the Kerdo index, rehabilitative potential from its basic constituent (morphophysiologicalindex). The motor-evacuational function of the stomach was studied with the use of a scintillation gamma-chamber, the gastric secretoryfunction by pH measurements. Results. Half of the patients in gr 2 presented with hypersympathicotony. The frequency of hypertonic form of gastric tone increased with durationof DM while the acid-producing and evacuational functions of the stomach decreased (as estimated by pH-measurement and gastroscintiographyrespectively). The propulsive function most significantly decreased in the pyloric part. The efficacy of rehabilitation of diabetic patients with gastrointestinalform of diabetic neuropathy was much lower than in those with preserved vegetative function of the stomach. Conclusion. Impairment of evacuational function of the stomach and duodenum with DM1 duration may be a cause of unstable blood glucose level.Hypomotor dyskinesia of the upper gastrointestinal tract due to DM1 and deficit of parasympathetic innervation occurs more frequently in patientswith low rehabilitative potential. Functional changes in the gastrointestinal tract of DM1 patients do not depend on the quality of compensation ofmetabolic disorders but correlate (r=-0.39) with DM duration. It is concluded that the gastrointestinal form of diabetic neuropathy impairs rehabilitativepotential of fhe patients.

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Raybould, Helen E., Jorg Glatzle, Carla Robin, James H. Meyer, Thomas Phan, Helen Wong, and Catia Sternini. "Expression of 5-HT3 receptors by extrinsic duodenal afferents contribute to intestinal inhibition of gastric emptying." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 3 (March 1, 2003): G367—G372. http://dx.doi.org/10.1152/ajpgi.00292.2001.

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Intestinal perfusion with carbohydrates inhibits gastric emptying via vagal and spinal capsaicin-sensitive afferent pathways. The aim of the present study was to determine the role of 1) 5-hydroxytryptamine (5-HT)3receptors (5-HT3R) in mediating glucose-induced inhibition of gastric emptying and 2) 5-HT3R expression in vagal and spinal afferents in innervating the duodenum. In awake rats fitted with gastric and duodenal cannulas, perfusion of the duodenum with glucose (50 and 100 mg) inhibited gastric emptying. Intestinal perfusion of mannitol inhibited gastric emptying only at the highest concentration (990 mosm/kgH2O). Pretreatment with the 5-HT3R antagonist tropisetron abolished both glucose- and mannitol-induced inhibition of gastric emptying. Retrograde labeling of visceral afferents by injection of dextran-conjugated Texas Red into the duodenal wall was used to identify extrinsic primary afferents. Immunoreactivity for 5-HT3R, visualized with an antibody directed to the COOH terminus of the rat 5-HT3R, was found in >80% of duodenal vagal and spinal afferents. These results show that duodenal extrinsic afferents express 5-HT3R and that the receptor mediates specific glucose-induced inhibition of gastric emptying. These findings support the hypothesis that enterochromaffin cells in the intestinal mucosa release 5-HT in response to glucose, which activates 5-HT3R on afferent nerve terminals to evoke reflex changes in gastric motility. The primary glucose sensors of the intestine may be mucosal enterochromaffin cells.

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Yi, S. Q., K. Ren, M. Kinoshita, N. Takano, M. Itoh, and N. Ozaki. "Innervation of Extrahepatic Biliary Tract, With Special Reference to the Direct Bidirectional Neural Connections of the Gall Bladder, Sphincter of Oddi and Duodenum inSuncus murinus, in Whole-Mount Immunohistochemical Study." Anatomia, Histologia, Embryologia 45, no. 3 (July 14, 2015): 184–88. http://dx.doi.org/10.1111/ahe.12186.

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Maggi, Carlo Alberto, Stefano Manzini, Sandro Giuliani, Paolo Santicioli, and Alberto Meli. "Extrinsic origin of the capsaicin-sensitive innervation of rat duodenum: possible involvement of calcitonin gene-related peptide (CGRP) in the capsaicin-induced activation of intramural non-adrenergic non-cholinergic neurons." Naunyn-Schmiedeberg's Archives of Pharmacology 334, no. 2 (October 1986): 172–80. http://dx.doi.org/10.1007/bf00505818.

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Kalogeris, Theodore J., V. Roger Holden, and Patrick Tso. "Stimulation of jejunal synthesis of apolipoprotein A-IV by ileal lipid infusion is blocked by vagotomy." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 5 (November 1, 1999): G1081—G1087. http://dx.doi.org/10.1152/ajpgi.1999.277.5.g1081.

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We examined the role of vagal innervation in lipid-stimulated increases in expression and synthesis of intestinal apolipoprotein A-IV (apoA-IV). In rats with duodenal cannulas and superior mesenteric lymph fistulas given duodenal infusions of lipid emulsion, vagotomy had no effect on either intestinal lipid transport, lymphatic apoA-IV output, or jejunal mucosal apoA-IV synthesis. In rats with jejunal Thiry-Vella fistulas, ileal lipid infusion elicited a twofold stimulation of apoA-IV synthesis without affecting apoA-IV mRNA levels; vagotomy blocked this increase in apoA-IV synthesis. Direct perfusion of jejunal Thiry-Vella fistulas produced 2- to 2.5-fold increases in both apoA-IV synthesis and mRNA levels in the Thiry-Vella segment; these effects were not influenced by vagal denervation. These results suggest two mechanisms whereby lipid stimulates intestinal apoA-IV production: 1) a vagal-dependent stimulation of jejunal apoA-IV synthesis by distal gut lipid that is independent of changes in apoA-IV mRNA levels and 2) a direct stimulatory effect of proximal gut lipid on both synthesis and mRNA levels of jejunal apoA-IV that is independent of vagal innervation.

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Hirose, T., and Y. Ito. "Excitatory and inhibitory responses of Oddi's sphincter in guinea pigs." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 4 (April 1, 1991): G615—G624. http://dx.doi.org/10.1152/ajpgi.1991.260.4.g615.

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We examined the intrinsic motor innervation of the guinea pig choledochoduodenal junction and actions of cholecystokinin octapeptide (CCK-OP) on contractile and membrane activity of circular and longitudinal smooth muscles from three different areas: close to the choledochal sphincter (I); central area in the ampulla (II); and close to the duodenal papilla (III). In response to electrical field stimulation, circular muscle strips showed an initial twitchlike contraction followed by relaxation in areas I and II and only a transient relaxation in the muscle strips prepared from area III. In the longitudinal strips, the regional differences in response to the field stimulation were not prominent, and biphasic twitchlike contractions were observed in areas I, II, and III. Electric field stimulation evoked excitatory junction potentials (EJPs), inhibitory junction potentials (IJPs), or biphasic membrane response (initial EJP followed by an IJP) in the circular and longitudinal smooth muscle cells. Prominent regional differences were observed in areas I, II, and III. Namely, in area III both the circular and longitudinal muscle layers IJPs predominated, whereas in area I the response was predominantly excitatory. CCK-OP (greater than 10-8M) evoked repetitive action potentials in the circular muscle cells, and CCK-OP increased the frequency of slow waves or the spontaneous action potentials in longitudinal muscle cells. CCK-OP enhanced the amplitude of the IJPs and EJPs in both muscle layers. It would thus appear that bile flow is controlled by complex combinations of contraction and relaxation of the smooth muscle that may be due to regional differences in excitatory and inhibitory innervations.

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Wang, Yu-Hua, Helen E. Raybould, and Jen Yu Wei. "Mechanosensitivity and chemosensitivity of vagal afferents innervating the duodenum in vitro." Gastroenterology 118, no. 4 (April 2000): A173. http://dx.doi.org/10.1016/s0016-5085(00)82771-7.

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Hobday, David I., Anthony R. Hobson, Sanchoy Sarkar, Paul L. Furlong, David G. Thompson, and Qasim Aziz. "Cortical processing of human gut sensation: an evoked potential study." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 2 (August 1, 2002): G335—G339. http://dx.doi.org/10.1152/ajpgi.00230.2001.

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The rectum has a unique physiological role as a sensory organ and differs in its afferent innervation from other gut organs that do not normally mediate conscious sensation. We compared the central processing of human esophageal, duodenal, and rectal sensation using cortical evoked potentials (CEP) in 10 healthy volunteers (age range 21–34 yr). Esophageal and duodenal CEP had similar morphology in all subjects, whereas rectal CEP had two different but reproducible morphologies. The rectal CEP latency to the first component P1 (69 ms) was shorter than both duodenal (123 ms; P = 0.008) and esophageal CEP latencies (106 ms; P = 0.004). The duodenal CEP amplitude of the P1-N1 component (5.0 μV) was smaller than that of the corresponding esophageal component (5.7 μV; P = 0.04) but similar to that of the corresponding rectal component (6.5 μV; P = 0.25). This suggests that rectal sensation is either mediated by faster-conducting afferent pathways or that there is a difference in the orientation or volume of cortical neurons representing the different gut organs. In conclusion, the physiological and anatomic differences between gut organs are reflected in differences in the characteristics of their afferent pathways and cortical processing.

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Ballesteros, M. A., J. D. Wolosin, D. L. Hogan, M. A. Koss, and J. I. Isenberg. "Cholinergic regulation of human proximal duodenal mucosal bicarbonate secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 261, no. 2 (August 1, 1991): G327—G331. http://dx.doi.org/10.1152/ajpgi.1991.261.2.g327.

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Cephalic-vagal stimulation affects a number of upper gastrointestinal secretory and motility events. The purpose of this study was to examine the role of vagal-cholinergic regulation on human proximal duodenal mucosal HCO-3 secretion. The duodenal bulb was isolated between balloons and perfused with 154 mM NaCl, and HCO-3 secretion was measured. Although cholinergic stimulation with bethanechol (50 micrograms.kg-1.h-1 iv) produced systemic effects, resting HCO-3 secretion was unchanged. Cephalic-vagal stimulation, induced by sham feeding, significantly increased duodenal HCO-3 secretion from a basal of 177 +/- 17 to 240 +/- 19 mumols.cm-1.h-1 (P less than 0.02). The response to sham feeding was approximately 50% of the peak response to acid-stimulated HCO-3 output. Atropine (22 micrograms/kg iv) inhibited basal HCO-3 secretion significantly (79 +/- 5%). However, the net incremental increases in duodenal mucosal HCO-3 secretion in response to luminal acidification and vagal stimulation were unaltered by atropine pretreatment. Additionally, indomethacin (100 mg po) failed to modify the response to vagal-stimulated HCO-3 secretion. These findings indicate that basal human proximal duodenal mucosal HCO-3 secretion is maintained largely by resting cholinergic innervation and is stimulated by cephalic-vagal stimulation. Furthermore, since the incremental HCO-3 responses to cephalic-vagal stimulation and luminal acidification were unaltered by atropine pretreatment, each is likely mediated by noncholinergic mechanisms.

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Cottrell, D. F., and J. G. Greenhorn. "THE VAGAL AND SPINAL INNERVATION OF THE GASTRO-DUODENAL JUNCTION OF SHEEP." Quarterly Journal of Experimental Physiology 72, no. 4 (October 10, 1987): 513–24. http://dx.doi.org/10.1113/expphysiol.1987.sp003093.

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Wen, J., E. Luque-De Leon, L. J. Kost, M. G. Sarr, and S. F. Phillips. "Duodenal motility in fasting dogs: humoral and neural pathways mediating the colonic brake." American Journal of Physiology-Gastrointestinal and Liver Physiology 274, no. 1 (January 1, 1998): G192—G195. http://dx.doi.org/10.1152/ajpgi.1998.274.1.g192.

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We have previously described a negative feedback loop that inhibits duodenal motility when nutrients are infused into the ileum and colon. In the present study, we examined the role of extrinsic innervation and plasma levels of peptide YY (PYY) in mediating this phenomenon. We perfused neurally intact ( n = 5 dogs) or extrinsically denervated ( n = 6 dogs) isolated loops of proximal colon with isomolar NaCl or a mixed-nutrient solution at 2 and 6 ml/min for 4 h during fasting or for 2 h beginning 15 min after a meal. Both rates of infusion with NaCl prolonged the cycle length of the duodenal migrating motor complex (MMC) in the group with neurally intact loops but not in the group with extrinsically denervated loops. Nutrient infusions increased the MMC cycle length in both groups. Integrated plasma concentrations of PYY were increased by nutrients but not by NaCl in both groups. These data suggest that increased volumes and unabsorbed nutrients in the proximal colon alter proximal small bowel motility. Volume-induced effects are mediated via extrinsic nerves, whereas nutrient-induced effects may be mediated by humoral factors, such as plasma PYY.

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Lemos, Sidney Pereira Pinto, José Luiz Martins, Patrícia Veruska Ribeiro Barbosa Lemos, Silvio Romero Gonçalves e. Silva, Fernando Leandro dos Santos, and Valdemiro Amaro da Silva Júnior. "Abnormalities of digestive tract innervation in rat fetus treated with ethylenethiourea." Acta Cirurgica Brasileira 27, no. 3 (March 2012): 244–50. http://dx.doi.org/10.1590/s0102-86502012000300007.

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PURPOSE: The pathophysiology of abnormalities associated with myenteric plexus lesions remains imperfectly understood. Such abnormalities have been correlated with subocclusive intestinal conditions in children with Hirschsprung's disease, cases of chronic constipation and, postoperatively, in cases of anorectal anomalies. This study evaluated abnormalities of the myenteric plexus in fetus from female rats that received ethylenethiourea. METHODS: Female rats were exposed to ethylenethiourea on the 11th day of pregnancy (experimental group) or to 0.9% physiological solution (control group). Abnormalities were only found in the experimental group. The digestive tract muscle layer was analyzed morphometrically and changes to the frequencies of nerve plexus cells and interstitial cells of Cajal were evaluated, using hematoxylin-eosin, S-100 protein, neuron-specific enolase and C-Kit, respectively. RESULTS: Muscle and skeletal abnormalities were observed in 100%, anorectal anomalies in 86%, absent tail in 71%, short tail in 29%, duodenal atresia in 5%, esophageal atresia in 5% and persistent omphalomesenteric duct in 5%. Histopathological analysis showed a thinner muscle layer associated with lower frequencies of ganglion cells and interstitial cells of Cajal, in all gastrointestinal tract. CONCLUSION: Severe nerve plexus abnormalities associated with muscle layer atrophy were observed throughout the gastrointestinal tract in newborn rats exposed to ethylenethiourea.

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Moore, Beverley A., David Kim, and Stephen Vanner. "Neural pathways regulating Brunner's gland secretion in guinea pig duodenum in vitro." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 5 (November 1, 2000): G910—G917. http://dx.doi.org/10.1152/ajpgi.2000.279.5.g910.

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This study examined the neural pathways innervating Brunner's glands using a novel in vitro model of acinar secretion from Brunner's glands in submucosal preparations from the guinea pig duodenum. Neural pathways were activated by focal electrical stimulation and excitatory agonists, and videomicroscopy was used to monitor dilation of acinar lumen. Electrical stimulation of perivascular nerves evoked large dilations that were blocked by TTX (1 μM) or the muscarinic receptor antagonist 4-diphenylacetoxy- N-(2-chloroethyl)-piperidine hydrochloride (1 μM). The nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium iodide (100 μM) had no effect, and the nerve-evoked responses were not inhibited by hexamethonium (200 μM). Dilations were abolished in preparations from chronically vagotomized animals. Activation of submucosal ganglia significantly dilated submucosal arterioles but not Brunner's glands. Effects of electrical stimulation of perivascular and submucosal nerves were not altered by guanethidine. Capsaicin and substance P also dilated arterioles but had no effect on Brunner's glands. Cholinergic (choline acetyltransferase-immunoreactive) nerve fibers were found in Brunner's glands. These findings demonstrate that Brunner's glands are innervated by cholinergic vagal fibers but not by capsaicin-sensitive or intrinsic enteric nerves.

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Yi, Shuang-Qin, Tetsuo Ohta, Koichi Miwa, Takashi Shimokawa, Keiichi Akita, Masahiro Itoh, Kensaku Miyamoto, and Shigenori Tanaka. "Surgical Anatomy of the Innervation of the Major Duodenal Papilla in Human and Suncus Murinus, From the Perspective of Preserving Innervation in Organ-saving Procedures." Pancreas 30, no. 3 (April 2005): 211–17. http://dx.doi.org/10.1097/01.mpa.0000158027.38548.34.

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Liu, Liansheng, Qian Li, Pratistha Tamrakar, Arun Sridhar, and Pankaj J. Pasricha. "334 Duodenal Innervation and the Metabolic Syndrome: Potential Role in Pathogenesis and as a Novel Therapeutic Target." Gastroenterology 150, no. 4 (April 2016): S79. http://dx.doi.org/10.1016/s0016-5085(16)30380-8.

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45

Bagaev, V. A., F. N. Makarov, V. L. Rybakov, �. �. Granstrem, E. V. Kopylov, E. B. Pluzhnichenko, S. I. Smirnov, and L. V. Filippova. "Localization of neurons innervating the upper portion of the duodenum in the motor nucleus of the vagus nerve." Neuroscience and Behavioral Physiology 22, no. 3 (May 1992): 230–36. http://dx.doi.org/10.1007/bf01196910.

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Allescher, H. D., S. Lu, E. E. Daniel, and M. Classen. "Nitric oxide as putative nonadrenergic noncholinergic inhibitory transmitter in the opossum sphincter of Oddi." Canadian Journal of Physiology and Pharmacology 71, no. 7 (July 1, 1993): 525–30. http://dx.doi.org/10.1139/y93-077.

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The sphincter of Oddi has a typical nonadrenergic noncholinergic inhibitory innervation; however, the transmitter of this inhibition has not been identified. The aim of the present study was to evaluate whether metabolites of the L-arginine – nitric oxide synthase pathway mediate neural inhibition in the sphincter of Oddi of the opossum. Electrical field stimulation at various frequencies (3, 5, and 10 pulses/s), performed in the presence of guanethidine (10−6 M) to exclude adrenergic responses, caused a slight, but significant excitatory response of the sphincter of Oddi. The responses were more pronounced at the duodenal side of the sphincter of Oddi than on the hepatic side. When the electrical field stimulation was repeated after blockading muscarinic receptors, using atropine (10−6 M), a potent inhibitory response was obtained. The inhibitory response to each of the various stimulation parameters was similar. Addition of L-arginine methyl ester (L-NAME, 2 × 10−4 M) abolished and reversed the inhibitory effect of electrical field stimulation, resulting in a potent stimulatory effect. Higher frequencies (5 and 10 pulses/s) were more potent in causing a stimulatory response than lower frequencies (3 pulses/s). The excitatory effect of electrical field stimulation was blocked or reversed to inhibition when the amino acid L-arginine (2 × 10−3 M) was added to the bath. In a second series of experiments, the inhibitory effect of electrical field stimulation in the presence of atropine and guanethidine was not prevented after the addition of methylene blue (5 × 10−5 M), a substance that, in vascular smooth muscle, has been demonstrated to block cyclic GMP dependent inhibitory responses. These data demonstrate that the sphincter of Oddi is characterized by an excitatory innervation that is partly cholinergic and partly nonadrenergic noncholinergic (NANC), while the NANC inhibitory response of this sphincter muscle is mediated by the release of endogenous nitric oxide or related compounds.Key words: nonadrenergic, noncholinergic, nitric oxide, L-arginine, sphincter of Oddi, methylene blue.

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Tiscornia, Osvaldo, Fabiana Lopez Mingorance, Selene Rodriguez, Gustavo Negri, and Patricia Tiscornia-Wasserman. "A Case Report of Biliary Colics Resembling Iterative Acute Pancreatitis (Stress Induced Through Vagal Innervation into Vaterian Duodeno-pancreas)." American Journal of Gastroenterology 111 (October 2016): S1295. http://dx.doi.org/10.14309/00000434-201610001-02564.

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48

Dunning, B. E., B. Ahren, R. C. Veith, and G. J. Taborsky. "Nonadrenergic sympathetic neural influences on basal pancreatic hormone secretion." American Journal of Physiology-Endocrinology and Metabolism 255, no. 6 (December 1, 1988): E785—E792. http://dx.doi.org/10.1152/ajpendo.1988.255.6.e785.

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Evidence for peptidergic innervation of the islets of Langerhans is increasing, yet the role of neuropeptides in mediating neurally induced changes of islet function is not clear. To determine if nonadrenergic transmitters make an important contribution to sympathetic neural effects on basal pancreatic hormone secretion, we examined the effect of local sympathetic nerve stimulation (SNS) on the output of immunoreactive insulin (IRI), immunoreactive glucagon (IRG), and somatostatin (SLI) from the duodenal lobe of the pancreas in situ in halothane-anesthetized dogs, under conditions where the actions of the classical transmitter norepinephrine (NE) should be blocked by propranolol (PROP) and yohimbine (YO). In the absence of adrenergic antagonists, SNS rapidly reduced the output of IRI (delta = -1.34 +/- 0.91 mU/min) and SLI (delta = -600 +/- 350 fmol/min) and stimulated that of IRG (delta = +1.39 +/- 0.57 ng/min). In the presence of PROP and YO, SNS induced similar changes of hormone secretion: delta IRI, -1.30 +/- 0.53 mU/min; delta SLI, -480 +/- 180 fmol/min; delta IRG = +1.89 +/- 0.63 ng/min. Because PROP and YO abolished the pancreatic effects of high dose infusions of NE (1 microgram.kg-1.min-1 iv), we suggest that the antagonists produced sufficient, combined adrenergic blockade at the level of the islet, and we conclude that a nonadrenergic neurotransmitter or modulator plays a major role in mediating sympathetic neural effects on basal islet hormone secretion.

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Ramalho-Santos, M., D. A. Melton, and A. P. McMahon. "Hedgehog signals regulate multiple aspects of gastrointestinal development." Development 127, no. 12 (June 15, 2000): 2763–72. http://dx.doi.org/10.1242/dev.127.12.2763.

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The gastrointestinal tract develops from the embryonic gut, which is composed of an endodermally derived epithelium surrounded by cells of mesodermal origin. Cell signaling between these two tissue layers appears to play a critical role in coordinating patterning and organogenesis of the gut and its derivatives. We have assessed the function of Sonic hedgehog and Indian hedgehog genes, which encode members of the Hedgehog family of cell signals. Both are expressed in gut endoderm, whereas target genes are expressed in discrete layers in the mesenchyme. It was unclear whether functional redundancy between the two genes would preclude a genetic analysis of the roles of Hedgehog signaling in the mouse gut. We show here that the mouse gut has both common and separate requirements for Sonic hedgehog and Indian hedgehog. Both Sonic hedgehog and Indian hedgehog mutant mice show reduced smooth muscle, gut malrotation and annular pancreas. Sonic hedgehog mutants display intestinal transformation of the stomach, duodenal stenosis (obstruction), abnormal innervation of the gut and imperforate anus. Indian hedgehog mutants show reduced epithelial stem cell proliferation and differentiation, together with features typical of Hirschsprung's disease (aganglionic colon). These results show that Hedgehog signals are essential for organogenesis of the mammalian gastrointestinal tract and suggest that mutations in members of this signaling pathway may be involved in human gastrointestinal malformations.

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Zhou, Shi-Yi, Yuanxu Lu, Il Song, and Chung Owyang. "Inhibition of gastric motility by hyperglycemia is mediated by nodose ganglia KATP channels." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 3 (March 2011): G394—G400. http://dx.doi.org/10.1152/ajpgi.00493.2010.

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The inhibitory action of hyperglycemia is mediated by vagal afferent fibers innervating the stomach and duodenum. Our in vitro studies showed that a subset of nodose ganglia neurons is excited by rising ambient glucose, involving inactivation of ATP-sensitive K+ (KATP) channels and leading to membrane depolarization and neuronal firing. To investigate whether nodose ganglia KATP channels mediate gastric relaxation induced by hyperglycemia, we performed in vivo gastric motility studies to examine the effects of KATP channel activators and inactivators. Intravenous infusion of 20% dextrose induced gastric relaxation in a dose-dependent manner. This inhibitory effect of hyperglycemia was blocked by diazoxide, a KATP channel activator. Conversely, tolbutamide, a KATP channel inactivator, induced dose-dependent gastric relaxation, an effect similar to hyperglycemia. Vagotomy, perivagal capsaicin treatment, and hexamethonium each prevented the inhibitory action of tolbutamide. Similarly, NG-nitro-l-arginine methyl ester, an inhibitor of nitric oxide synthase, also blocked tolbutamide's inhibitory effect. To show that KATP channel inactivation at the level of the nodose ganglia induces gastric relaxation, we performed electroporation of the nodose ganglia with small interfering RNA of Kir6.2 (a subunit of KATP) and plasmid pEGFP-N1 carrying the green fluorescent protein gene. The gastric responses to hyperglycemia and tolbutamide were not observed in rats with Kir6.2 small interfering RNA-treated nodose ganglia. However, these rats responded to secretin, which acts via the vagal afferent pathway, independently of KATP channels. These studies provide in vivo evidence that hyperglycemia induces gastric relaxation via the vagal afferent pathway. This action is mediated through inactivation of nodose ganglia KATP channels.

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Journal articles on the topic 'Duodenum – Innervation'

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