Submucosal plexus alone integrates motor activity and epithelial transport in rat jejunum

1990 ◽  
Vol 259 (4) ◽  
pp. G593-G598 ◽  
Author(s):  
N. A. See ◽  
B. Greenwood ◽  
P. Bass

It has been well established in several mammalian species, including humans, that contractions of jejunal smooth muscle correlate temporally with increases in mucosal ion transport. Furthermore, this correlation is abolished through local application of neurotoxins, suggesting interaction of enteric neurons. The purpose of this study was to determine whether the myenteric plexus is involved in this correlation. In the rat jejunum in vivo, we simultaneously measured phasic changes in intraluminal pressure and transmural potential difference (PD) as indicators of smooth muscle motor activity and epithelial ion transport, respectively. We compared the temporal association of these parameters in control animals with animals in which either the extrinsic nerves only or the extrinsic nerves and the myenteric plexus of a 5-cm jejunal segment had been ablated 30 days previously. A one-to-one coupling between muscle contractions and transmural PD fluctuations was observed in all animals; ablation of the extrinsic and/or myenteric neurons did not eliminate this correlation. We conclude that, in the rat jejunum, the submucosal plexus alone can integrate the reflex that couples ion secretion to muscle contraction.

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Michał Bulc ◽  
Jarosław Całka ◽  
Łukasz Zielonka ◽  
Michał Dąbrowski ◽  
Katarzyna Palus

AbstractGastrointestinal neuropathy in diabetes is one of numerous diseases resulting in abnormal functioning of the gastrointestinal tract (GIT), and it may affect any section of the GIT, including the descending colon. In the gastrointestinal system, the neurons are arranged in an interconnecting network defined as the enteric nervous system (ENS) which includes the myenteric plexus and the submucosal plexuses: inner and outer. Regular functioning of the ENS is determined by normal synthesis of the neurotransmitters and neuromodulators. This paper demonstrates the effect of hyperglycaemia on the number of enteric neurons which are immunoreactive to: neural isoform of nitric oxide synthase (nNOS), vasoactive intestinal peptide (VIP), galanin (GAL), calcitonin gene-related peptide (CGRP) and cocaine amphetamine-regulated transcript (CART) in the porcine descending colon. It was demonstrated that there was a statistically significant increase in the number of neurons within the myenteric plexus immunoreactive to all investigated substances. In the outer submucosal plexus, the CART-positive neurons were the only ones not to change, whereas no changes were recorded for nNOS or CART in the inner submucosal plexus. This study is the first study to discuss quantitative changes in the neurons immunoreactive to nNOS, VIP, GAL, CGRP and CART in the descending colon in diabetic pigs.


Author(s):  
Daniel E Levin ◽  
Arabinda Mandal ◽  
Mark A Fleming ◽  
Katherine H Bae ◽  
Brielle Gerry ◽  
...  

Abstract The role of enteric neurons in driving intestinal peristalsis has been known for over a century. However, in recent decades, scientists have begun to unravel additional complex interactions between this nerve plexus and other cell populations in the intestine. Investigations into these potential interactions is complicated by a paucity of tractable models of these cellular relationships. Here, we describe a novel technique for ex vivo coculture of enteroids, so called “mini-guts,” in juxtaposition to the longitudinal muscle myenteric plexus (LMMP). Key to this system, we developed a LMMP culture media that: 1) allows the LMMP to maintain ex vivo peristalsis for 2 weeks along with proliferation of neurons, glia, smooth muscle and fibroblast cells, and 2) supports the proliferation and differentiation of the intestinal stem cells into enteroids complete with epithelial enterocytes, Paneth cells, goblet cells and enteroendocrine cells. Importantly, this technique identifies a culture condition that supports both the metabolic needs of intestinal epithelium as well as neuronal elements, demonstrating the feasibility of maintaining these two populations in a single culture system. This sets the stage for experiments to better define the regulatory interactions of these two important intestinal cell populations.


2002 ◽  
Vol 119 (6) ◽  
pp. 533-543 ◽  
Author(s):  
Guangju Ji ◽  
Robert J. Barsotti ◽  
Morris E. Feldman ◽  
Michael I. Kotlikoff

Smooth muscle cells undergo substantial increases in length, passively stretching during increases in intraluminal pressure in vessels and hollow organs. Active contractile responses to counteract increased transmural pressure were first described almost a century ago (Bayliss, 1902) and several mechanisms have been advanced to explain this phenomenon. We report here that elongation of smooth muscle cells results in ryanodine receptor–mediated Ca2+ release in individual myocytes. Mechanical elongation of isolated, single urinary bladder myocytes to ∼120% of slack length (ΔL = 20) evoked Ca2+ release from intracellular stores in the form of single Ca2+ sparks and propagated Ca2+ waves. Ca2+ release was not due to calcium-induced calcium release, as release was observed in Ca2+-free extracellular solution and when free Ca2+ ions in the cytosol were strongly buffered to prevent increases in [Ca2+]i. Stretch-induced calcium release (SICR) was not affected by inhibition of InsP3R-mediated Ca2+ release, but was completely blocked by ryanodine. Release occurred in the absence of previously reported stretch-activated currents; however, SICR evoked calcium-activated chloride currents in the form of transient inward currents, suggesting a regulatory mechanism for the generation of spontaneous currents in smooth muscle. SICR was also observed in individual myocytes during stretch of intact urinary bladder smooth muscle segments. Thus, longitudinal stretch of smooth muscle cells induces Ca2+ release through gating of RYR. SICR may be an important component of the physiological response to increases in luminal pressure in smooth muscle tissues.


Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 263
Author(s):  
Andrea Toschi ◽  
Giorgia Galiazzo ◽  
Andrea Piva ◽  
Claudio Tagliavia ◽  
Gemma Mazzuoli-Weber ◽  
...  

An important piece of evidence has shown that molecules acting on cannabinoid receptors influence gastrointestinal motility and induce beneficial effects on gastrointestinal inflammation and visceral pain. The aim of this investigation was to immunohistochemically localize the distribution of canonical cannabinoid receptor type 1 (CB1R) and type 2 (CB2R) and the cannabinoid-related receptors transient potential vanilloid receptor 1 (TRPV1), transient potential ankyrin receptor 1 (TRPA1), and serotonin receptor 5-HT1a (5-HT1aR) in the myenteric plexus (MP) of pig ileum. CB1R, TRPV1, TRPA1, and 5-HT1aR were expressed, with different intensities in the cytoplasm of MP neurons. For each receptor, the proportions of the immunoreactive neurons were evaluated using the anti-HuC/HuD antibody. These receptors were also localized on nerve fibers (CB1R, TRPA1), smooth muscle cells of tunica muscularis (CB1R, 5-HT1aR), and endothelial cells of blood vessels (TRPV1, TRPA1, 5-HT1aR). The nerve varicosities were also found to be immunoreactive for both TRPV1 and 5-HT1aR. No immunoreactivity was documented for CB2R. Cannabinoid and cannabinoid-related receptors herein investigated showed a wide distribution in the enteric neurons and nerve fibers of the pig MP. These results could provide an anatomical basis for additional research, supporting the therapeutic use of cannabinoid receptor agonists in relieving motility disorders in porcine enteropathies.


2005 ◽  
Vol 98 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
Jay S. Naik ◽  
Scott Earley ◽  
Thomas C. Resta ◽  
Benjimen R. Walker

Chronic obstructive pulmonary diseases, as well as prolonged residence at high altitude, can result in generalized airway hypoxia, eliciting an increase in pulmonary vascular resistance. We hypothesized that a portion of the elevated pulmonary vascular resistance following chronic hypoxia (CH) is due to the development of myogenic tone. Isolated, pressurized small pulmonary arteries from control (barometric pressure ≅ 630 Torr) and CH (4 wk, barometric pressure = 380 Torr) rats were loaded with fura 2-AM and perfused with warm (37°C), aerated (21% O2-6% CO2-balance N2) physiological saline solution. Vascular smooth muscle (VSM) intracellular Ca2+ concentration ([Ca2+]i) and diameter responses to increasing intraluminal pressure were determined. Diameter and VSM cell [Ca2+]i responses to KCl were also determined. In a separate set of experiments, VSM cell membrane potential responses to increasing luminal pressure were determined in arteries from control and CH rats. VSM cell membrane potential in arteries from CH animals was depolarized relative to control at each pressure step. VSM cells from both groups exhibited a further depolarization in response to step increases in intraluminal pressure. However, arteries from both control and CH rats distended passively to increasing intraluminal pressure, and VSM cell [Ca2+]i was not affected. KCl elicited a dose-dependent vasoconstriction that was nearly identical between control and CH groups. Whereas KCl administration resulted in a dose-dependent increase in VSM cell [Ca2+]i in arteries taken from control animals, this stimulus elicited only a slight increase in VSM cell [Ca2+]i in arteries from CH animals. We conclude that the pulmonary circulation of the rat does not demonstrate pressure-induced vasoconstriction.


1989 ◽  
Vol 256 (3) ◽  
pp. H630-H640 ◽  
Author(s):  
M. J. Davis ◽  
R. W. Gore

Longitudinal response gradients in the microcirculation may in part be explained in terms of the length-tension relationship of vascular smooth muscle at different points along the vascular tree. To test this hypothesis, four branching orders of arterial vessels (20-80 microns ID) were dissected from the hamster cheek pouch and cannulated with concentric micropipettes. Intraluminal pressure was monitored with a servo-null micropipette, and arteriolar dimensions were measured using a videomicrometer. All arterioles developed spontaneous tone in physiological saline solution. Pressure-diameter curves were recorded for maximally activated vessels and for passive vessels. Maximal active wall tension varied nearly threefold, but maximal active medial wall stress (approximately 4 x 10(6) dyn/cm2) varied only approximately 20% between the different vessel orders. These data support the concept that smooth muscle cells from vessels of different sizes are mechanically similar but do not completely explain the longitudinal response gradients reported in the cheek pouch microcirculation. An analysis of the effect of arteriolar wall buckling suggests that the luminal folds that develop at short vessel radii may broaden the peak of the active stress-length curve and extend the pressure range over which arterioles are most sensitive to physical and chemical stimuli.


2009 ◽  
Vol 297 (4) ◽  
pp. G716-G725 ◽  
Author(s):  
Xuan-Zheng Shi ◽  
Sushil K. Sarna

We tested the hypothesis that spontaneous release of vasoactive intestinal peptide (VIP) from enteric neurons maintains homeostasis in smooth muscle function in mild inflammatory insults and that infusion of exogenous VIP has therapeutic effects on colonic smooth muscle dysfunction in inflammation. In vitro experiments were performed on human colonic circular smooth muscle tissues and in vivo on rats. The incubation of human colonic circular smooth muscle strips with TNF-α suppressed their contractile response to ACh and the expression of the pore-forming α1C subunit of Cav1.2 channels. VIP reversed both effects by blocking the translocation of NF-κB to the nucleus and its binding to the κB recognition sites on hα1C1b promoter. The translocation of NF-κB was inhibited by blocking the degradation of IκBβ. Induction of inflammation by a subthreshold dose of 17 mg/kg trinitrobenzene sulfonic acid (TNBS) in rats moderately decreased muscularis externa concentration of VIP, and it had little effect on the contractile response of circular smooth muscle strips to ACh. The blockade of VIP and pituitary adenylate cyclase-activating peptide receptors 1/2 during mild inflammatory insult significantly worsened the suppression of contractility and the inflammatory response. The induction of more severe inflammation by 68 mg/kg TNBS induced marked suppression of colonic circular muscle contractility and decrease in serum VIP. Exogenous infusion of VIP by an osmotic pump reversed these effects. We conclude that the spontaneous release of VIP from the enteric motor neurons maintains homeostasis in smooth muscle function in mild inflammation by blocking the activation of NF-κB. The infusion of exogenous VIP mitigates colonic inflammatory response and smooth muscle dysfunction.


2014 ◽  
Vol 86 (6) ◽  
pp. 18-30 ◽  
Author(s):  
L. G. Babich ◽  
◽  
S. G. Shlykov ◽  
S. O. Kosterin ◽  
◽  
...  

Gastric dysrhythmias are abnormal myoelectrical signals originating from the stomach. As recorded from cutaneous or serosal electrodes, bradygastrias range from 0 to 2.5 cycles per minute (cpm). Bradygastrias and mixed gastric dysrhythmias are reviewed in detail in Chapter 8. Tachygastrias range from 3.75 to l0.0cpm. The normal duodenal pacesetter potential ranges from 12 to 14 cpm. In this chapter, tachygastrias are reviewed in detail. Multiple metabolic mechanisms and neural-hormonal pathways influence gastric myoelectrical activity. The normal activities of enteric neurons, smooth muscle, hormones, and extrinsic nerves influence the ongoing activity of the interstitial cells of Cajal (ICCs), the pacemaker cells of the stomach. In healthy subjects, the frequency of gastric myoelectrical activity may vary from approximately 2.5 to 3.7cpm, depending on specific circumstances or provocative tests (Fig. 7.1). Specific diseases and disorders, with their specific pathophysiologies, may adversely affect gastric myoelectrical activity and are associated with gastric dysrhythmias. For example, many patients with type I and II diabetes have gastric dysrhythmias, and in healthy subjects, hyperglycemia itself produces gastric dysrhythmias. Gastric dysrhythmias occur when the ICCs are damaged or dysfunctional or when enteric neurons, circular smooth muscle cells (and perhaps longitudinal muscle activity), and extrinsic nerve activity from the parasympathetic and sympathetic nervous system input to the stomach are abnormal. Endocrine, neurocrine, and paracrine activities may also affect interstitial cells, enteric neurons, and smooth muscle and thereby affect gastric myoelectrical rhythms,21 shifting electrical activity to bradygastrias (0-2.5cpm) or tachygastrias (3.7- l0.0cpm) as shown in Figure 7.1. All of these influences interact to maintain normal gastric myoelectrical activity during baseline periods and in response to meals or other provocative stimuli. Stimuli that provoke stomach neuromuscular activity range from motion and the illusion of motion to emotionally challenging situations (disgust, anger) to the cephalic phase of digestion (vagal activation in the presence of appetizing food) to the relaxation, contraction, and coordination of stomach neuromuscular responses during and after the ingestion of a wide variety of solid and liquid foodstuffs. Thus, there are many gut-brain and brain-gut interactions to consider when evaluating gastric myoelectrical events during EGG recordings at baseline and after provocative stimuli.


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