SEARCH · PubMed Health

Results for “MYENTERIC PLEXUS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources

PubMed1990

Altered carbachol-induced contractile responses of rat jejunal smooth muscle following local myenteric plexus ablation.

Alterations in smooth muscle responsiveness and neural pathways in adjacent tissue may occur after local myenteric denervation. The in vitro contractile responses of both longitudinal and circular muscle to the mixed muscarinic and nicotinic cholinergic agonist carbachol were determined 15, 30, and 45 days after localized myenteric plexus ablation. Denervated longitudinal muscle exhibited decreased responsiveness to carbachol at all times examined. Denervated circulated muscle was initially supersensitive, but with time became subsensitive. These changes probably reflect the loss of the nicotinic (neuronal) component of the action of carbachol. Muscle orad to the site of denervation appeared subsensitive, while muscle caudad to the lesion was supersensitive (circular) or unaffected (longitudinal). These results suggest that there are changes in ascending and descending neural pathways. Alterations in the cholinergic responsiveness of intestinal smooth muscle, both at and beyond the site of myenteric plexus ablation, may result in altered intestinal motility that could lead to functional obstruction.

Animals↗

PubMed2005

Evaluation of the effect of age on cannabinoid receptor functionality and expression in guinea-pig ileum longitudinal muscle-myenteric plexus preparations.

Cannabinoid drugs exert a wide range of biological effects and are currently under study for their multiple potential therapeutic uses. Cannabinoids reduce gastrointestinal (GI) motility and this is mediated by the CB1 cannabinoid receptor (CB1R) present in the myenteric neurones. GI motility can also be affected by a variety of pathophysiological situations, including ageing. The purpose of this work was to study the influence of age on the functionality and expression of CB1R in the myenteric plexus. Ileal longitudinal muscle-myenteric plexus (LMMP) preparations from young, adult and old guinea-pigs were used in two sets of experiments: in vitro assessment of the inhibitory cannabinoid effect upon electrically stimulated contractions and immunohistochemical quantification of myenteric neurones expressing CB1R. LMMP preparations responded to the synthetic cannabinoid WIN 55,212-2, and the endogenous cannabinoid ligand anandamide in an age-independent manner. The total number of CB1R-immunoreactive (IR) myenteric neurones, which included at least part of the motor neurones to the longitudinal smooth muscle, decreased in proportion to the general neuronal population; however, the proportion of CB1R-IR neurones was preserved in old animals. These data may justify the preservation of the effectiveness of the cannabinoids in the isolated guinea-pig ileum. This age-related independency of CB1R expression and effect on GI motility could be of interest if cannabinoids are to be used therapeutically.

Aging↗

PubMed1985

Hypoganglionosis of the myenteric plexus with normal Meissner's plexus: a new variant of colonic ganglion cell disorders.

A 16-year-old girl with a history of achalasia of the lower esophagus was investigated for progressive constipation since the age of five years. Normal ganglion cells of the Meissner's plexus were found in a mucosal rectal biopsy. Manometric studies showed absence of the normal rectosphincteric relaxation reflex. A long posterior rectal myectomy was performed in which no ganglion cells were found between the muscular layers. The patient underwent a rectosigmoid resection with a low anastomosis according to Duhamel. In the resected bowel, a normal Meissner's plexus was again found while marked hypoganglionosis of the myenteric plexus was evident. Intranuclear inclusion bodies in Schwann cells and scattered inflammatory cells were noteworthy. This case may be an example of an acquired hypoganglionosis localized to the myenteric plexus.

Adolescent↗

PubMed1989

Effect of 7-chloro kynurenic acid on glycine modulation of the N-methyl-D-aspartate response in guinea-pig myenteric plexus.

The glycine modulation of the N-methyl-D-aspartate (NMDA) response in guinea-pig myenteric plexus was investigated by using D-serine and 7-chloro kynurenic acid as a glycine agonist and antagonist, respectively. D-serine caused a concentration-dependent enhancement of the NMDA response, an effect which was competitively inhibited by 7-chloro kynurenic acid (pA2 = 6.0). In addition, 7-chloro kynurenic acid induced a concentration-dependent, non-competitive inhibition of the NMDA response per se, even in the absence of added D-serine. This inhibition was fully reversed by exogenous D-serine, suggesting that this effect was also due to the occupancy of the glycine site. These results emphasize the usefulness of the guinea-pig myenteric plexus for studying the function of the NMDA receptor complex.

Animals↗

PubMed1999

Nitric oxide synthase-containing neurons in the myenteric plexus of the rat gastrointestinal tract: distribution and regional density.

Nitrergic (NO) neurons play crucial inhibitory roles in the control of gut motility. Variations in the density of these neurons within the gastrointestinal tract (GI) may provide useful functional information, but, most surveys available have employed limited and/or highly localized samples. It remains unclear to what extent (a) NO neurons are concentrated disproportionately in particular GI regions, or (b) variations in NO cell number merely reflect changes in overall myenteric neuron density. This experiment surveyed the distributions of neuronal nitric oxide synthase-positive (NOS+) and other myenteric neurons in the GI tract, using immunohistochemical and Cuprolinic blue counterstaining techniques. Adjustable sampling grids superimposed on wholemounts were used to investigate the topographic patterns in the stomach (90 sampling sites; 45 per side) and proximal duodenum (63 loci). We present four major findings: First, variations were detected in the number of NOS+ neurons in specific regions of the stomach (e.g., corpus > antrum approximately equal to forestomach) and along both longitudinal (oral > anal) and circumferential (mesenteric > antimesenteric) axes in the duodenum. Second, the variations in NOS+ neuronal counts within each organ covaried with the total number of myenteric neurons at different locations (stomach, r=0.77; duodenum, r=0.59), suggesting that local myenteric plexus density is a factor determining NOS+ cell concentrations. Third, in contrast to such a principle of covariation within each organ, NOS+ neurons constituted a consistently smaller proportion of gastric (20%) than of duodenal (28%) myenteric plexus neurons, suggesting that a second principle controls the characteristic percentages of the myenteric plexus that express NOS in different organs. Fourth, the regional samples were used to extrapolate the overall number of NOS+ and total myenteric cells in the rat stomach (43,000; 217,000) and first 3.5 cm of the small intestine (29,000; 103,000). These results, taken together, also suggest that the surveying protocol used is capable of detecting subtle differences in cellular distributions, thus providing a practical strategy for investigating patterns of chemical phenotypes within the GI tract.

Animals↗

PubMed1988

Interaction of forskolin with the effect of atropine on [3H]acetylcholine secretion in guinea-pig ileum myenteric plexus.

1. Secretion of [3H]acetylcholine was studied in the guinea-pig ileum longitudinal muscle-myenteric plexus preparation. The transmitter stores of the cholinergic nerves were labelled by pre-incubation with [3H]choline. The preparation was mounted in an organ bath and superfused with Tyrode solution containing hemicholinium-3 and eserine. [3H]Acetylcholine secretion was evoked by electrical stimulation (0.5 Hz, 150 shocks). 2. 8-Bromo cyclic AMP, the adenylate cyclase activator forskolin, and the cyclic nucleotide phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine enhanced the [3H]acetylcholine secretion in a concentration-dependent manner. The values of 'maximal enhancement' calculated were similar, viz. 200-300% of control. 3. 8-Bromo cyclic GMP reduced the [3H]acetylcholine secretion. 4. The 'maximal enhancement' of 3-isobutyl-1-methylxanthine was not altered by the presence of forskolin (25 mumol/l) suggesting a common mechanism of action, i.e. elevation of endogenous cyclic AMP levels. 5. The muscarinic acetylcholine receptor antagonist atropine enhanced the [3H]acetylcholine secretion with a 'maximal enhancement' of 506% of control. Presence of neither forskolin (25 mumol/l) nor 3-isobutyl-1-methylxanthine (5 mmol/l) altered the 'maximal enhancement' for atropine. 6. In contrast, atropine (1 mumol/l) and 4-aminopyridine (0.5 mmol/l) additively enhanced the [3H]acetylcholine secretion. 7. The results suggest that neuronal cyclic AMP may be involved in muscarinic acetylcholine receptor-mediated control of [3H]acetylcholine secretion in guinea-pig ileum myenteric plexus.

1-Methyl-3-isobutylxanthine↗

PubMed1993

Actions of nitric oxide-generating sodium nitroprusside in myenteric plexus of guinea pig small intestine.

Sodium nitroprusside (NaNP) was used as a donor of nitric oxide (NO) to investigate actions of NO on electrical and synaptic behavior of single myenteric neurons in guinea pig small intestine. NaNP (10 microM-1 mM) did not affect resting membrane properties of the neurons, except for an occasional decrease in input resistance and hyperpolarization attributable to suppression of excitatory transmitter release. NaNP did not alter fast nicotinic neurotransmission but suppressed noncholinergic slow excitatory postsynaptic potentials (slow EPSPs) in a concentration-dependent manner. Pretreatment with either methylene blue or oxyhemoglobin reduced the inhibitory action of NaNP on the slow EPSPs. Slow EPSP-like responses to microejected substance P or 5-hydroxytryptamine were unaffected by NaNP. The nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester, did not affect resting membrane excitability or excitatory synaptic events in any of the myenteric neurons. The results suggest that NO may not be released extensively as a neurotransmitter at synapses within the myenteric plexus. If myenteric neurons are exposed to NO released from nonneural sources, then the principal action is expected to be presynaptic inhibition of slow synaptic excitation.

Animals↗

PubMed1982

Chronic idiopathic intestinal pseudo-obstruction caused by a degenerative disorder of the myenteric plexus: the use of Smith's method to define the neuropathology.

In this paper we report the pathologic basis of chronic idiopathic intestinal pseudo-obstruction in a patient who had a subtotal colectomy and ileorectal anastomosis for severe obstipation. Conventional light microscopy of the resected intestine showed an increased thickness of the longitudinal muscle, minimal amounts of smooth muscle fibrosis, and normal smooth muscle cells. The morphology of the myenteric plexus was difficult to interpret with this technique, but quantification of colonic neurons revealed a significantly decreased number compared with controls. Silver stains of the myenteric plexus by Smith's method showed: (a) patchy loss of nerve tracts with replacement by Schwann cells, (b) degeneration and decreased numbers of both argryophilic and argyrophobic neurons, (c) fragmentation and dropout of many axons, and (d) increased thickness and disorganized spatial arrangement of other axons. The pathology of this intestinal neuropathy could be missed by conventional light microscopy and may be apparent only when a silver technique is used to visualize the myenteric plexus.

Colon↗

PubMed1992

Ultrastructure of the developing myenteric plexus of chicken small intestine.

The present ultrastructural study established the main morphological events that occur during the myenteric plexus formation in the chicken duodenum from the 7th day of incubation (E7) up to hatching, with special attention to the appearance of different axon profiles and synaptic contacts. Transmission electron microscopy revealed that the compartmentalization of the enteric mesenchyma into outer and inner zones precedes the sequential morphological maturation of the crest derived cells during myenteric plexus formation. On E7, a slender neuropil was present in the migrating cell clusters, but all the crest derived cells were uniform. In the following stages, the neuronal and enteroglial cells were distinguishable. The first significant sign of neuronal maturation was the morphological heterogeneity in the vesicle population on E11. Progressive changes in the synaptogenesis were identified, and the axosomatic synapses were characteristic around hatching. On E18, a transient direct muscle-ganglion contact with the circular muscle layer was observed, in addition to the permanent ganglionar contact to the longitudinal layer of the muscularis externa.

Animals↗

PubMed1993

[Morphology of the myenteric plexus of the small intestine in patients with liver cirrhosis].

BACKGROUND: Patients with liver cirrhosis develop small bowel dysmotility of unknown etiology. Morphological features in the enteric nervous system and the intestinal smooth muscle may shed light on pathophysiology of the gut motility disturbances in this disease. AIM: To investigate the morphology of the myenteric plexuses and smooth muscle layers of the small intestine in patients with liver cirrhosis. PATIENTS AND METHODS: Full thickness biopsies of duodenum, jejunum and ileum from seven cirrhotic patients and seven controls were stained with several techniques, including silver impregnation. Neuronal counting and light microscopy studies were stained performed. RESULTS: The neuronal count was not significantly different in patients with cirrhosis compared to controls in duodenal samples (1.6 +/- 0.4 cel/mm vs 1.6 +/- 0.2 cel/mm), jejunal tissue (1.2 +/- 0.3 cel/mm vs 1.4 +/- 0.2 cel/mm), and in ileal specimens (0.8 +/- 0.3 cel/mm vs 0.9 +/- 0.2 cel/mm). In both groups, evidence of fibrosis or inflammation in myenteric plexuses and in smooth muscle was not found. Also, intestinal neuronal dysplasia was absent in cirrhotic patients as in controls. CONCLUSION: These results suggest that small bowel dysmotility in patients with liver cirrhosis is not related to structural changes in myenteric plexuses or in intestinal smooth muscle noted by light microscopy.

Adult↗

PubMed1990

The myenteric plexus regulates cell growth in rat jejunum.

The roles of the myenteric and extrinsic nerves in the control of proliferation and cell growth in the rat jejunum were studied. The myenteric plexus and/or the extrinsic nerves in a segment of rat jejunum were ablated by serosal application of the surfactant benzyldimethyltetradecylammonium chloride or by crushing the nerves passing through the mesentery, respectively. Ablation of both myenteric and extrinsic nerves, but not the extrinsic nerves alone, resulted in a significant increase in the mitotic rate of the crypt-epithelial cells and in the size of VIP-immunoreactive neurons in the submucosal plexus. The increased mitotic rate was correlated with an increase in the weight of the mucosa per unit length of gut and in the villus length and crypt depth. Neither extrinsic denervation alone nor serosal application of saline had any effect on these parameters. Our results suggest that the myenteric plexus is able to influence the rate of cell proliferation and cell growth in the rat jejunum.

Animals↗

PubMed1989

Impaired acetylcholine release from the myenteric plexus of Trichinella-infected rats.

We examined the release of acetylcholine (ACh) from jejunal longitudinal muscle-myenteric plexus preparations in noninfected control rats and in rats infected 6, 23, or 40 days previously with Trichinella spiralis. ACh release was assessed by preincubating the tissue with [3H]choline and measuring the evoked release of tritium. The uptake of 3H was significantly less in tissue from T. spiralis-infected rats compared with control. In tissues from either infected or control animals, electrical field stimulation (30 V, 0.5 ms, 10 Hz for 1 min), or veratridine (6-30 microM) induced 3H release that was tetrodotoxin sensitive. Depolarization by KCl (25-75 mM) also caused 3H release, but this was only partially reduced by tetrodotoxin. Radiochromatographic analysis indicated evoked release of 3H to be almost entirely [3H]ACh. In rats infected 6 days previously with T. spiralis, [3H]ACh release induced by KCl, veratridine, and field stimulation were decreased at least 80%. The suppression of [3H]ACh release induced by veratridine or KCl was fully reversible after 40 days postinfection, but field-stimulated responses remained approximately 50% of control values. These results indicate that T. spiralis infection in the rat is accompanied by a reversible suppression of ACh release from the longitudinal muscle-myenteric plexus of the jejunum.

Acetylcholine↗

PubMed1981

Neuropeptides in the gut: quantification and characterization of cholecystokinin octapeptide-, bombesin- and vasoactive intestinal polypeptide-like immunoreactivities in the myenteric plexus of the guinea-pig small institute.

The localization of CCK8-, bombesin- and VIP-like immunoreactivities in the myenteric plexus of the guinea pig small intestine has been studied by radioimmunoassay of extracts of longitudinal muscle strips obtained with and without adherent myenteric plexus; concentrations were compared with those in other regions of the gut. In innervated strips of longitudinal muscle of ileum there was approximately 14 pmol/g CCK8-, 32 pmol/g bombesin- and 135 pmol/g VIP-like immunoreactivity; concentrations were reduced by over 70% in denervated strips. Gel filtration and ion exchange chromatography indicated that over 80% of CCK immunoreactivity was due to CCK8; no evidence was found of significant amounts of smaller COOH-terminal fragments. Bombesin immunoreactivity occurred in two forms, the major one resembling the amphibian tetradecapeptide in its elution from gel filtration columns. Immunoreactive VIP differed markedly from porcine VIP in immunochemical and chromatographic properties; the data suggest that guinea pig VIP is less basic than porcine VIP and that the two peptides differ in structure in their NH2-terminal regions. Some functional implications of these findings are discussed.

Animals↗

PubMed1975

Endogenous acetylcholine release and labelled acetylcholine formation from [3H]choline in the myenteric plexus of the guinea-pig ileum.

The spontaneous release of acetylcholine (ACh) from the guinea-pig myenteric plexus - longitudinal muscle preparation superfused at a constant rate in the presence of physostigmine was 10 nmol-g-1-h-1. This release was decreased to one-third by tetradotoxin or by MnCl2 and increased 2.5 times by 0.1 Hz and 20 times by 16 Hz stimulation. The formation of [3H]ACh from [3H]choline increased from 3 to 33 nmol-g(-1)-h(-1) when the concentration of [3H]choline was increased from 1 muM to 50 muM. The rate of [3H]ACh formation was not affected by tetrodotoxin, MnCl2, or physostigmine in the absence of stimulation. It was increased by 50% by 0.1 Hz and by 100% by 16 Hz stimulation during the first 9 min of exposure to [3H]choline but not subsequently. The myenteric plexus - longitudinal muscle preparation contains 200 nmol/g choline. Results suggest that the apparent small [3H]ACh formation from low concentrations of [3H]choline is due to the dilution of [3H]choline by endogenous choline. The major part of [3H]ACh formation appears to be due to the intracellular turnover of ACh while the evoked release of [3H]ACh appears to originate from a small pool.

Acetylcholine↗

PubMed1990

An electrophysiological study of the projections of putative sensory neurons within the myenteric plexus of the guinea pig ileum.

Conduction of action potentials in the processes of AH (afterhyperpolarizing) neurons has been examined in the myenteric plexus of the guinea-pig small intestine. AH neurons are a morphologically distinct class of myenteric neurons in which the action potentials are followed by long lasting afterhyperpolarizations and which usually lack fast synaptic inputs. These neurons have large smooth cell bodies and several long processes. We have used electrophysiological methods, combined with intracellular injection of the fluorescent dye 5(6)-carboxyfluorescein, to examine the directions of projection and lengths of axons of AH neurons. AH neurons of the myenteric plexus projected circumferentially in both directions from the cell soma for electrophysiologically determined average distances of 0.74 +/- 0.05 mm. Thus, the neurons span about 1.5 mm of the circumference of the intestine. About one quarter of the AH neurons had one, or rarely two, processes that ran anally after initially projecting circumferentially. All processes conducted action potentials, with average conduction velocities of 0.23 +/- 0.02 ms-1.

Action Potentials↗

PubMed1982

Myenteric plexus in a freshwater teleost intestine. I. Quantitative study of nerve cells.

The number of nerve cells in the myenteric plexus of a freshwater teleost (Pimelodus maculatus) was obtained with the aid of statistical methods. 1. The density of neurons/cm2 was the following: 91,142 in the duodenum; 93,133 in the ileum and 82,857 in the rectum. These 3 portions have not showed statistically significant differences. 2. The mean surface area of the intestine being 48 cm2, the total number of neurons in myenteric plexus of the duodenum, ileum and rectum was calculated to be 4,274,112.

Animals↗

PubMed2001

Two-dimensional alterations of myenteric plexus in jejunoileal atresia.

PURPOSE: The purpose of this report is to investigate changes in the myenteric plexus associated with the dilated proximal segment of jejunoileal atresia (JA). Two-dimensional morphologic changes in the myenteric nerve plexuses were investigated using whole-mount preparation. METHODS: Proximal (P) and distal (D) intestinal segments from 7 cases with JA and control (C) segments from 5 postmortem neonates were investigated. The circumference of the jejunoileal segments was measured after fixation. Antibodies for protein gene product 9.5 and neurofilament protein were used in whole-mount preparation. The sizes of neural networks were calculated by measuring the longest circular distance in a neural network (x) and the longest longitudinal distance (y), and the width of the internodal strands (i) with a videomicrometer. RESULTS: Median circumference of the segments was 8.5 in P, 2.0 in D, and 2.0 cm in C. The neural networks in P were expanded longitudinally as well as circularly (x = 817.10 microm, y = 561.26, i = 31.04: median) while comparing them to those in D (x = 431.40 microm y = 288.07, i = 26.05) or C (x = 285.03 microm y = 372.20, c = 1113.57, i = 32.39). The nerve plexus was less expanded than the intestinal wall. CONCLUSIONS: Proximal intestinal segments showed a restructuring that resulted in mild hypoplasia of the enteric nerve plexuses in the proximal segments. The less expansion of the myenteric nerve plexus seen in the proximal bowel in infants with JA suggests a histologic basis for the efficacy of tapering or plication of the dilated bowel.

Case-Control Studies↗

PubMed1998

Role of protein kinase C in the release of [3H]acetylcholine from myenteric plexus treated with vesamicol.

The present experiments investigated the release of [3H]acetylcholine ([3H]ACh) from the guinea pig myenteric plexus treated with 2-(4-phenylpiperidino)cyclohexanol (vesamicol), a drug that impairs ACh accumulation by synaptic vesicles. Ouabain, an Na+-K+ ATPase inhibitor, released [3H]ACh synthesised in the presence of (-)-vesamicol, while electrical field stimulation or KCl depolarisation were not effective to release the transmitter in this condition. The effect of ouabain was Ca2+-dependent and in the presence of (-)-vesamicol it was blocked by calphostin C, an inhibitor of protein kinase C (PKC). In addition, stimulation of kinase C activity by a phorbol ester, but not by its inactive isomer, prevented (-)-vesamicol from interfering with the release of [3H]ACh in electrically-stimulated myenteric plexus, similar to the effect of ouabain. We conclude that release of [3H]ACh induced by ouabain in the presence of (-)-vesamicol depends on PKC activation.

Acetylcholine↗