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Results for “MYENTERIC PLEXUS”

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At least 433 records · Page 24Linked to original sources

PubMed1989

Deficient neurogenic innervation of the myenteric plexus with normal submucous plexus involving the entire small and large bowel.

A newborn presented with a picture of intestinal obstruction. Multiple biopsies of the small and large bowel showed an unusual neurogenic innervation. The myenteric plexus of Auerbach was severely depleted of ganglion cells and nerve fibers, while the submucous plexus of Meissner was normally innervated. An ileostomy failed to function and extended trial with experimental smooth muscle stimulant (Cisapride) was equally ineffective. The patient was finally treated by a myectomy from the duodenum to the descending colon with a sigmoid colostomy. This procedure, coupled with a Nissen fundoplication, stopped the vomiting and allowed normal defecation through the colostomy. The patient is presently taking increasing increments of oral fluids with a concomitant decrease in the volume of parenteral nutrition. The myectomy initiated marked hypertrophy of the muscularis mucosa. Could this muscular hypertrophy account for the improvement in bowel function? Possible etiology will be discussed. We caution that rectal submucosal suction biopsy alone may be misleading if normal ganglion cells and nerve fibers are found, yet the patient's clinical symptoms fail to improve. A full thickness bowel wall biopsy is then recommended.

Ganglia, Parasympathetic↗

PubMed2001

Neuron count reevaluation in the myenteric plexus of chagasic megacolon after morphometric neuron analysis.

This study was made with the objective of reevaluating the colon denervation in chronic Chagas' disease. The diameters of neuron perikaryons of the myenteric plexus were measured on paraffin sections in a ring from the sigmoid in Chagas' disease patients, 17 with and 10 without megacolon and in 10 non-chagasic controls. All neurons were counted in ten en-echelon sections. Neuron hypertrophy only occurred in the group with megacolon, and the average increase in diameter was 69.3%. This could generate an error factor in the neuron count by increasing the probability of neurons being seen in a greater number of histological sections. The original result of the neuron count gave medians of 1264, 1961, and 2665 in the groups of chagasic patients with megacolon, without megacolon, and in the control, respectively. The denervation was greater than 55% in only seven megacolon cases (41.2%). After applying a correction factor, the median in the group with megacolon was 746, and the denervation was greater than 55% in 13 cases (76.5%). This occurrence demonstrates the need to apply a correction factor when the neuron count in chagasic megacolon is being evaluated and in the other pathologies where neuron hypertrophy may be found.

Adult↗

PubMed1992

Interactions of lithium with the adrenergic system in electrically-stimulated guinea pig myenteric plexus isolated preparations. Actions of a phosphodiesterase inhibitor.

The possible involvement of lithium in the mechanism of action of norepinephrine has been studied in electrically-stimulated preparations isolated from guinea pig myenteric plexus. Results show that concentrations of lithium above 0.5 x 10(-2) M significantly inhibit the norepinephrine effect. The results obtained when preparations were preincubated with alpha-adrenergic blocking agents (phenoxybenzamine and phentolamine) suggest a beta-adrenergic action of lithium since these substances induced 74% and 37% inhibition of the lithium effects, respectively. When preparations were preincubated with beta-adrenergic blocking agents (propranolol, toliprolol, atenolol and sotalol) the action of lithium was unchanged. A phosphodiesterase inhibitor also led to 50% inhibition of the lithium effects. These results, together with the fact that the adenylate cyclase cAMP system is linked directly to the beta-adrenoceptors, suggest that the inhibitory action of lithium on norepinephrine, in this preparation, is related to its beta-adrenergic action, which agrees with the results obtained in brain by other authors.

1-Methyl-3-isobutylxanthine↗

PubMed1994

Expression of cytokines in the longitudinal muscle myenteric plexus of the inflamed intestine of rat.

BACKGROUND/AIMS: Trichinella spiralis infection in the rat produces mucosal injury and inflammation and causes changes in muscle function and neurotransmitter release in the longitudinal muscle myenteric plexus (LMMP). Whether these changes in LMMP reflect the production of inflammatory mediators in the LMMP remains unknown. The objective of this study was to investigate the profile of interleukins (IL) 1-alpha, 1-beta, and 6 and tumor necrosis factor (TNF) alpha in the LMMP of infected rats. Because muscle changes are T-cell dependent, we also studied the cytokine profile in infected athymic rats. METHODS: Cytokine messenger RNA (mRNA) was examined using semiquantitative polymerase chain reaction, and protein was measured by enzyme-linked immunosorbent assay, radioimmunoassay, or bioassay. RESULTS: There was increased expression of IL1-alpha and -beta, IL-6, and TNF-alpha mRNA and protein in the LMMP of both euthymic and athymic infected rats. Increased expression of each cytokine was observed by 24 hours postinfection and, in the case of IL1-beta and TNF-alpha, remained elevated by day 6 postinfection. CONCLUSIONS: Mucosal injury following T. spiralis infection is accompanied by enhanced expression of proinflammatory cytokines in the LMMP. The expression of IL1-, IL-6, and TNF-alpha in infected athymic rats suggests that these cytokines do not contribute to the changes in muscle growth or contraction but may mediate the previously described changes in neurotransmitter release in this model.

Animals↗

PubMed1987

Effect of lanthanum on the release of acetylcholine from the myenteric plexus and on its activation by ouabain and electrical stimulation.

The effect of lanthanum ions (La3+) on the release of acetylcholine (ACh) from longitudinal muscle strips of the guinea pig ileum with the myenteric plexus attached was investigated. After an exposure of the tissue to 2 mM LaCl3 for 18 min the rate of ACh release was increased approximately eightfold and the increased release lasted for more than 100 min. The augmented release of ACh was accompanied by enhanced synthesis. At the end of the experiments (102 min after LaCl3 had been removed), when the release of ACh was still more than six times higher than in controls, the content of ACh was the same in La3+-treated and untreated tissues. Electrical field stimulation failed to cause a further increase in the release of ACh from La3+-pretreated preparations whereas ouabain released considerable more ACh when compared to controls. It is concluded from this difference that electrical stimulation and ouabain release ACh from different pools.

Acetylcholine↗

PubMed1986

A case of eosinophilic meningo-encephalitis accompanied by eosinophilic inflammation of the myenteric plexus in Hodgkin's disease.

A case of Hodgkin's disease with eosinophilia in the cerebrospinal fluid without blood eosinophilia is presented. An additional remarkable feature was the finding of eosinophilia in Auerbach's myenteric plexus. Cerebrospinal fluid eosinophilia is usually associated with blood eosinophilia and this is often caused by helminthic infections of the CNS. The finding of cerebrospinal fluid eosinophilia without blood eosinophilia in any patient with Hodgkin's disease should point the physician to the possibility of a localization of tumour in the CNS.

Adult↗

PubMed2003

Effect of protein and vitamin B deficiency on the morpho-quantitative aspects of the myenteric plexus of the descending colon of adult rats.

We carried out this work with the purpose of studying the effects of protein and vitamin B deficiency on the morphologic and quantitative aspects of the myenteric plexus of the descending colon of adult Rattus norvegicus. Twenty-eight rats were divided in two groups, one of them receiving chow with 22% protein level (control) and the other fed with chow having 8% protein level without vitamin B supplementation, during 120 days. Whole-mounts of the descending colon were prepared and stained with Giemsa, NADH-diaphorase and NADPH-diaphorase. The undernourished rats had a body weight 11.84% less than the control group. Relative to the controls, the experimental group had a colonic area 48% smaller, 51.9% less Giemsa-stained neurons, 28.3% less NADH-diaphorase positive neurons and 24.2% less NADPH-diaphorase positive neurons.

Animals↗

PubMed1995

Tonic modulation of neurotransmitter release in the guinea-pig myenteric plexus: effect of mu and kappa opioid receptor blockade and of chronic sympathetic denervation.

We have studied the effects of mu- and kappa-opioid receptor blockade on endogenous acetylcholine and noradrenaline overflow from the myenteric plexus of the guinea-pig isolated colon. Cyprodime (putative mu-selective antagonist) and nor-binaltorphimine (kappa-selective antagonist) had a concentration-dependent facilitatory effect on both acetylcholine and noradrenaline overflow. Moreover, in colonic specimens obtained from sympathetically denervated animals, the effect of opioid antagonists on acetylcholine overflow was significantly higher with respect to normal preparations. Evidence is thus given in favour of an involvement of mu- and kappa-opioid receptor pathways in the tonic modulation of neurotransmitter release at the colonic level. Enhanced sensitivity to the effect of mu and kappa antagonists after chronic sympathetic denervation is strongly suggestive for the existence of a functional link between opioid and adrenergic pathways in this model.

Acetylcholine↗

PubMed1989

Contribution of external Ca2+ to the modulation by prostaglandin E2 of the release of acetylcholine from the myenteric plexus of guinea pig ileum.

The effects of external concentration of Ca2+ [( Ca2+]o) on the modulation by indomethacin (IND) or prostaglandin E2 (PGE2) of the evoked release of acetylcholine (ACh) were investigated in the myenteric plexus of guinea pig ileum. An increase in the [Ca2+]o from 0.45 to 3.6 mM depressed both the spontaneous and the nicotine-induced release of ACh, while the releases of ACh induced by electrical-field stimulation (EFS) or by high K+ were augmented. IND and PGE2 did not modify the release of ACh induced by EFS and high K+, at any given [Ca2+]o tested. The nicotine-induced release of ACh was significantly inhibited by IND with no relation to [Ca2+]o, and these inhibitory effects of IND were prevented by PGE2. At 0.45 mM [Ca2+]o, the extent of the recovery by PGE2 was less potent than those at other [Ca2+]o. IND inhibited the spontaneous release of ACh at lower [Ca2+]o, and such inhibition was not observed in the presence of PGE2. Thus, the modulatory actions of PGE2 on the spontaneous and the nicotine-induced release of ACh may depend partially on [Ca2+]o.

Acetylcholine↗

PubMed1980

Evidence that substance P is a neurotransmitter in the myenteric plexus.

Substance P (SP) is an undecapeptide originally isolated from the gut and since shown to occur within neurones in several parts of the peripheral and central nervous systems. Immunohistochemical studies indicate an exceedingly dense network of SP-containing nerves within the myenteric plexus of the guinea pig ileum. These nerves are intrinsic to the gut wall and can release SP to contract the longitudinal muscle layer. We have previously shown that SP directly depolarizes myenteric neurones and that this depolarization has a time course and ionic mechanism similar to the slow excitatory postsynaptic potential (e.p.s.p.) which can be produced by electrical stimulation of presynaptic nerves within the myenteric ganglia. We wondered whether SP might mediate this slow synaptic potential. We report here that the SP depolarization and the slow e.p.s.p. are reversibly depressed by chymotrypsin, an enzyme which degrades SP, although the responses to acetylcholine, serotonin and an unknown hyperpolarizing transmitter are unaffected. The results provide direct evidence that a peptide can mediate chemical transmission between neurones in the mammalian nervous system.

Animals↗

PubMed1983

A quantitative study on the myenteric plexus of the distal end of the duodenum and the proximal part of the jejunum.

4 necropsy specimens taken from adult individuals were used in order to estimate the density of nerve cell bodies of the myenteric plexus in the last distal 5 cm of the duodenum and the proximal 5 cm of the jejunum (including the duodenojejunal flexure), that were subdivided into parts of approximately 1 cm and stained by Giemsa's method according to Barbosa (1970). Except for the first 2 parts, an increase of the neuron number was observed toward the duodenojejunal flexure, the greatest being at this point, and then decreasing progressively. The first duodenal parts, which corresponds approximately to the intersection of the mesenteric artery with the duodenum, showed the same neuron density as the duodenojejunal flexure. In this paper the 2 parts with higher neuron density were related to functional sphincteric zones, previously described.

Adult↗

PubMed2000

Calcium channels coupled to depolarization-evoked glutamate release in the myenteric plexus of guinea-pig ileum.

Glutamate is the major excitatory neurotransmitter in the CNS. The recent characterization of glutamate as a neurotransmitter in the enteric nervous system opened a new line of investigation concerning the role of glutamate in that system. The present study aimed to further characterize the enteric glutamate release and the calcium channels coupled to it. For this study the myenteric plexus-longitudinal muscle of guinea-pig ileum was stimulated with potassium chloride or with electrical pulses. The released glutamate was detected by spectrofluorimetry. Laser scanning confocal microscopy was used for analysis of immunolabeled enteric tissue for co-localization studies of calcium channels (N- and P/Q-type) and glutamate transporters (EAAC1). Here we report the effects of known Ca(2+)-channel blockers on glutamate release evoked by KCl-depolarization or electrical stimulation in the myenteric plexus. We find that N-type Ca(2+) channels control a major portion of evoked glutamate release from this system, with a very small contribution from L-type Ca(2+) channels. Moreover, alpha(1A)-like (P-type Ca(2+) channel) and alpha(1B)-like (N-type Ca(2+ )channel) immunoreactivity co-localized with glutamate transporters in the myenteric plexus. In addition, KCl-evoked or electrically stimulated glutamate release was sensitive to omega-agatoxin IVA, in a frequency-dependent manner, suggesting that P-type channels are also coupled to the release of glutamate. We, thus, conclude that both N-type and P-type Ca(2+) channels control most of the evoked glutamate release from the enteric nervous system, as also occurs in some parts of the CNS.

Amino Acid Transport System X-AG↗

PubMed1984

Constipation and congenital disorders of the myenteric plexus.

Full-thickness muscle biopsies have been taken from patients with severe disabling chronic constipation that has not responded to conservative measures. Assessment by neurohistochemical techniques has revealed that a range of neuronal dysplasias of the myenteric plexus are responsible in many cases; these include aganglionosis (Hirschsprung's disease), hypoganglionosis and hyperganglionosis. In cases considered unlikely to be Hirschsprung's disease on clinical grounds, the procedure used has often been anorectal myectomy; this has not only provided tissue for diagnosis but has also been of therapeutic value in most cases of hypoganglionosis and some cases reported as 'normal'.

Adult↗

PubMed1997

Neurochemical coding in the myenteric plexus of the upper gastrointestinal tract of hibernating hamsters.

As part of our investigation of the plasticity of autonomic nerves in physiological and pathological conditions, we have examined the effect of hibernation on the neurochemical content of myenteric nerves and nerve cell bodies of the upper gastrointestinal tract of the non-seasonal hibernator, the golden hamster. Age matched hamsters kept at room temperature and those kept at 5 degrees C but which failed to hibernate, were used as controls. Possible changes in nerve fibres and nerve cell bodies containing the general neuronal marker, protein gene product 9.5, the peptides, vasoactive intestinal polypeptide, substance P (SP) and calcitonin gene-related peptide (CGRP), the catecholamine synthesizing enzyme tyrosine hydroxylase and the enzyme responsible for synthesizing nitric oxide, nitric oxide synthase, were examined in the oesophagus, proventriculus and proximal and distal stomach of the golden hamsters using immunohistochemical techniques. The results of the present study revealed a significant increase in the number of nerve cell bodies and density of nerve fibres containing SP-immunoreactivity and increased number of CGRP-immunoreactive cell bodies but not the other markers examined in the proximal stomach and proventriculus. In contrast, there was no change in the distribution of any of the neuroactive substances examined in the myenteric plexus of the oesophagus and distal stomach. It is suggested that the change in the environment of the hibernating hamsters perturbs the normal digestive physiology in the proximal stomach and proventriculus that is reflected by the selective changes in SP- and CGRP-containing enteric nerves; these changes may be part of protective reflex mechanisms to the environmental changes resulting from hibernation, where upgrading of nerve cell bodies expressing CGRP and SP has occurred.

Animals↗

PubMed1994

Effect of longitudinal muscle-myenteric plexus removal and indomethacin on the response to tachykinin NK-2 and NK-3 receptor agonists in the circular muscle of the guinea-pig ileum.

1. The effect of removal of the longitudinal muscle-myenteric plexus (LM-MP) and/or indomethacin (10 microM) on the response to the tachykinin NK-2 receptor selective agonist, [beta Ala8]NKA(4-10), or to the NK-3 receptor selective agonist, senktide, was investigated by measuring mechanical activity (isotonic recording) of circular muscle (ring preparation) of the guinea-pig ileum. 2. Indomethacin (10 microM) increased the percentage of ileal rings displaying spontaneous activity, either intact or LM-MP-free. The response to senktide (10 nM and 1 microM) was lower in LM-MP-free than in intact ileal rings, either in the absence or presence of indomethacin. The response to a low concentration (10 nM) of [beta Ala8] NKA (4-10) was enhanced in LM-MP-free rings and by indomethacin. 3. In intact ileal rings, the response to senktide was unaffected by atropine (3 microM) alone or by the tachykinin NK-2 receptor antagonist MEN 10,376 (10 microM) alone while it was reduced by the combined administration of the two antagonists. The response to senktide was greatly reduced by tetrodotoxin (TTX, 1 microM). Senktide-induced contractions (10 nM) were also reduced by the blocker of N-type voltage-sensitive calcium channels, omega-contoxin (CTX, 0.1 microM). 4. In about 30% of preparations tested, an inhibitory response (decrease in spontaneous activity) to 10 nM senktide, was disclosed in CTX-treated intact ileal rings. This inhibitory effect was TTX-sensitive. 5. In LM-MP-free ileal rings, the response to senktide was abolished or reduced by atropine and MEN 10,376, alone or in combination, and was also reduced or abolished by TTX and CTX. 6. The response to [beta Ala8]NKA (4-10) was inhibited by MEN 10,376, in both intact and LM-MP-free ileal rings while it was unaffected by atropine, TTX or CTX. 7. These results indicate that indomethacin pretreatment induces a regular background activity for studying the motor response to tachykinins in the circular muscle of the ileum, probably by blocking the formation of relaxant prostanoids. A further increase in sensitivity to direct smooth muscle stimulation (NK-2 receptor agonist) can be obtained by removal of the LM-MP. The response to NK-3 receptor stimulation is diminished but not abolished by removal of the LM-MP, suggesting that NK-3 receptors are located on neuronal bodies of myenteric neurons, but possibly also at other sites (possibly, nerve terminals).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1987

Somatostatin inhibits cAMP-mediated cholinergic transmission in the myenteric plexus.

The mechanism by which somatostatin acts to modulate cholinergic transmission is not clear. In this study we investigated the role of the adenosine 3',5'-cyclic monophosphate (cAMP) system in mediating cholinergic transmission in the guinea pig myenteric plexus and examined the ability of somatostatin to alter acetylcholine (ACh) release stimulated by various cAMP agonists. Forskolin, 8-bromo-cAMP, vasoactive intestinal peptide (VIP), and cholera toxin each stimulated the release of [3H]ACh in a dose-related manner. Addition of theophylline enhanced the release of [3H]ACh stimulated by these cAMP agonists. In contrast 2',5'-dideoxyadenosine, an inhibitor of adenylate cyclase, antagonized the action of forskolin, VIP, and cholera toxin but had no effect on that evoked by 8-bromo-cAMP. These observations suggest that cAMP may serve as a physiological mediator for ACh release from myenteric neurons. Somatostatin inhibited release of [3H]ACh evoked by various cAMP agonists in a dose-related manner. Maximal inhibition, observed in the presence of 10(-6) M somatostatin was 48 +/- 5, 47 +/- 9, and 43 +/- 12% of control for forskolin-, VIP-, and cholera toxin-evoked release of [3H]ACh. In contrast somatostatin at 10(-6) M inhibited only 20 +/- 5% of the release of [3H]ACh stimulated by 8-bromo-cAMP. Pretreatment with pertussis toxin antagonized the inhibitory effect of somatostatin on the release of [3H]ACh evoked by forskolin, VIP, or cholera toxin but had no effect on the inhibitory action of somatostatin on the release of [3H]ACh evoked by 8-bromo-cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1976

Functional intestinal obstruction due to deficiency of argyrophil neurones in the myenteric plexus. Familial syndrome presenting with short small bowel, malrotation, and pyloric hypertrophy.

In 3 infants functional intestinal obstruction, associated with a short small intestine, malrotation, and pyloric hypertrophy, was shown to be due to failure of development of the argyrophil myenteric plexus, with the absence of ongoing peristalsis. 4 infants with similar clinical features have been described previously, and there is evidence for an autosomal recessive mode of inheritance of this syndrome.

Female↗

PubMed1993

Interleukin 1 beta-induced increase in substance P in rat myenteric plexus.

BACKGROUND: Substance P (SP) is increased in the inflamed intestine of Trichinella spiralis-infected rats, but the underlying mechanism is unknown. Interleukin 1 beta (IL-1 beta) messenger RNA and protein is expressed in the longitudinal muscle-myenteric plexus (LM-MP) of this model. Thus, the purpose of the study was to examine the ability of human recombinant IL-1 beta (hrIL-1 beta) to increase SP in LM-MP preparations from the intestine of noninfected rats. METHODS: LM-MP preparations were incubated with hrIL-1 beta, and immunoreactive SP (IR-SP) was assessed in the tissues by radioimmunoassay or immunohistochemistry. RESULTS: hrIL-1 beta increased IR-SP in the tissue in a time- and concentration-dependent manner, being maximal after 6 hours at a concentration of 10 ng/mL. The IR-SP could be depleted by scorpion venom, and immunohistochemistry revealed increased staining for SP within nerves of the LM-MP. The action of IL-1 beta was dependent on protein synthesis, was receptor mediated, and was not due to endotoxin contamination of the cytokine preparation. CONCLUSIONS: hrIL-1 beta stimulates the synthesis of SP in myenteric nerves of rat intestine.

Animals↗