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PubMed1989

Quinoxalines interact with the glycine recognition site of NMDA receptors: studies in guinea-pig myenteric plexus and in rat cortical membranes.

1. The effects of several quinoxalines, including 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and 6,7,dinitroquinoxaline-2,3-dione (DNQX), and of two kynurenates, kynurenate (KYNA) and 7-Clkynurenate (7-Cl-KYNA), have been evaluated on the N-methyl-D-aspartate (NMDA) receptors present in the guinea-pig ileum myenteric plexus preparation and on the strychnine-insensitive [3H]-glycine binding sites of cortical membranes. 2. Quinoxalines and kynurenates antagonized in a non-competitive manner L-glutamate-induced contraction. Their IC50s were (in microM): 5 for 7-Cl-KYNA, 7.5 for 6,7-Cl-3-hydroxy-2-quinoxaline carboxylate (6,7-Cl-HQCA), 20 for DNQX, 50 for CNQX, 76 for KYNA and 125 for 3-hydroxy-2-quinoxaline carboxylate (HQCA). 3. Glycine (5-50 microM) completely reversed the antagonism displayed by both quinoxalines and kynurenates. The interaction between glycine and the tested compounds appeared to be competitive in nature. 4. Quinoxalines and kynurenates displaced, in a concentration-dependent manner, [3H]-glycine from its strychnine-insensitive binding sites present in rat cortical membranes. Their IC50s for this action were (in microM): 0.45 for 7-Cl-KYNA, 0.6 for 6,7-Cl-HQCA, 2.4 for DNQX, 3.5 for CNQX, 20 for KYNA and 40 for HQCA. 5. When the IC50s for the displacement effect of [3H]-glycine binding were plotted against the IC50s obtained in the myenteric plexus, a significant correlation was found. 6. These data show that quinoxalines and kynurenates may antagonize the responses to L-glutamate by interacting with the glycine recognition sites of the NMDA receptor ion channel complex.

Animals↗

PubMed1994

Immaturity of the myenteric plexus is the aetiology of meconium ileus without mucoviscidosis: a histopathologic study.

The most common aetiology of meconium ileus is a deficiency in trypsin activity caused by cystic fibrosis. The pathogenesis of meconium ileus without mucoviscidosis is less well understood, although a number of causative factors have been suggested. The symptoms and clinical course of nine patients with meconium ileus without mucoviscidosis were reviewed, and the myenteric plexus of a surgical specimen of intestine was examined histologically and cytometrically. The nuclei of the intramural ganglion cells were much smaller than were seen in normal newborn infants. The nuclear areas resembled those seen in fetuses of 5-6 months gestational age, but the number of ganglion cells approached normal. This immaturity of the ganglia was observed both in the contracted distal ileum and dilated proximal ileum. Patients with an ileostomy passed solid faeces for about 1 to 2 months postoperatively, after which time the faeces became watery. The intramural ganglia were mature at the time of ileostomy closure. We conclude that immaturity of the myenteric plexus in the ileum and colon seems to be the main aetiologic factor in meconium ileus without mucoviscidosis.

Cytodiagnosis↗

PubMed1984

Dynorphin inhibition of the neurotensin contractile activity on the myenteric plexus.

Nanomolar concentrations of neurotensin caused a dose-dependent contraction of the longitudinal muscle layer of the guinea-pig ileum. The contractile activity of neurotensin was partially blocked by tetrodotoxin or atropine, indicating that a component of the neurotensin-mediated contraction is indirect in nature and likely involves the release of endogenous acetylcholine from nervous terminals in the myenteric plexus. Dynorphin and related peptide fragments also blocked in part the neurotensin contraction; the potency of this opioid peptide was about the same as that of atropine. Other peptides and alkaloids tested for ability to block the neurotensin contractures included the enkephalins, beta-endorphin, normorphine and the ketocyclazocines; all these opioids inhibited in a dose-dependent fashion the neuronal component of the excitatory effect of neurotensin. The potency of these compounds to reduce the contractions of neurotensin showed good correlation with the potency of these agents to depress by 50% the electrically evoked neuromuscular twitches in the same tissue (r = 0.99); in these tests dynorphin was found to be the most potent of the endogenous opioid-like peptides. The dynorphin blockade was selective to the excitatory effect of neurotensin because the opioid peptide did not antagonize the contractile action of acetylcholine, histamine, substance P, angiotensin II, bradykinin, Ba++ or K+ ions. In addition, somatostatin, vasointestinal peptide, gastrin or adenosine did not modify the potency of neurotensin whereas thyrotropin releasing hormone and epinephrine caused a modest doubling of the neurotensin EC50. The inhibitory action of dynorphin was reduced in the presence of naloxone, suggesting that the interaction involved opiate receptors. Morphine tolerance was not extended to the inhibitory action of dynorphin as evidenced by the finding that the potency of dynorphin-(1-13) to block the neurotensin responses was increased after chronic morphine exposure. In contrast, the potency of dynorphin-(1-13) was significantly reduced in tissues rendered tolerant to the action of ketocyclazocine or ethylketocyclazocine, suggesting that the action of dynorphin could be partially mediated via occupation of K-opiate receptors. Thus, a cholinergic-neuronal component activated by neurotensin on the myenteric plexus appears to be under the inhibitory influence of opiate receptors, suggesting that dynorphin may play a role in the modulation of cholinergic synapses on the enteric nervous system.

Animals↗

PubMed1996

Presence of gonadotropin-releasing hormone (GnRH) receptor mRNA in rat myenteric plexus cells.

Idiopathic neuromuscular disease of the gastrointestinal tract (functional bowel disease) is thought to result from the malfunction of neurons within the enteric nervous system. Gonadotropin-releasing hormone (GnRH) analogs have recently been shown to organize the disordered motility patterns typical in these patients and to produce significant, long-term symptomatic improvement. To determine whether GnRH analogs might bind to an endogenous enteric nervous system GnRH receptor, reverse transcription-polymerase chain reaction (RT-PCR) was performed using cultured neonatal rat enteric neuron RNA and rat GnRH receptor primers. A PCR product of the predicted size was cloned and nucleotide sequence analysis demonstrated that the myenteric plexus PCR product encoded a portion of the GnRH receptor sequence previously identified in rat pituitary. These results suggest that cells in the myenteric plexus express GnRH receptors that may bind exogenously administered GnRH analogs. The expression of GnRH receptors in enteric neurons would provide an explanation for the effectiveness of GnRH analogs in treatment of idiopathic neuromuscular disease of the gastrointestinal tract.

Amino Acid Sequence↗

PubMed2001

Megacystis secondary to myenteric plexus pathology. Presentation of two cases.

Herein, 2 cases of megacystis secondary to myenteric plexus pathology are reported. Unlike the entity of visceral myopathy, there was ganglion cell loss both in the bladder and in the colon of these 2 cases. Moreover, they did not present any gastrointestinal symptoms. Megacystis was the common pathology in these patients, whereas 1 of them suffered from unilateral vesicoureteral reflux. We could not find any similar report dealing with this phenomenon up to this time in the literature.

Adolescent↗

PubMed1985

Ultrastructural identification of VIP-containing nerve fibres in the myenteric plexus of the rat ileum.

Vasoactive intestinal polypeptide (VIP)-containing nerve fibres of myenteric plexus of the rat ileum were investigated using the pre-embedding peroxidase-antiperoxidase technique for electron microscopy. The VIP-positive fibres were characterized by a predominance of spherical agranular vesicles with a diameter of 40-55 nm. The immunoprecipitate was largely localized on the vesicle membrane. Large granular vesicles (100-144 mm) containing labelled dense cores were also present within labelled nerve profiles. Quantitative data indicate that the vesicles appeared in the following proportions: 93% small agranular vesicles and 7% large granular vesicles.

Animals↗

PubMed1985

A study of the myenteric plexus of the congenital aganglionosis rat (spotting lethal).

The entire bowel of a mutant strain of rats, the congenital aganglionosis rat (spotting lethal), was investigated using the acetylcholinesterase reaction and immunohistochemical staining for tyrosine hydroxylase and substance P in whole-mount preparations. The histology of the bowel of mutant rats was also studied by light- and electron microscopy. In all examined mutant rats, a constricted region of intestine followed a dilated region of the bowel. In 29 cases constricted segments extended from rectum to distal ileum; in 3 cases from rectum to middle colon. In controls the myenteric plexus appeared as a mesh-work consisting of ganglion strands and internodal strands, showing a rather regular ladder-like pattern from duodenum to rectum. The myenteric plexus of mutants was very different from that of controls, showing conspicuous regional differences. Even in the duodenum, where there was no macroscopical disorder, the plexus showed an irregular pattern, the meshes varying greatly in size and shape. Ganglion strands were shorter than those in controls. The plexus in the dilated segment gradually decreased in density, finally disappearing above the proximal terminal of the constricted segment. In some areas below this transition, i.e., the anal portion of the constricted segment in 29 cases (long constricted segment type only), there were neither ganglion cells nor nerve fibers except for scarcely distributed tyrosine hydroxylase-immunoreactive nerve fibers. In the distal part of the upper colon some fine nerve bundles appeared to run irregularly. These nerve bundles gradually increased in number and mixed with thicker nerve bundles in the lower portion of the colon. Finally, at the level of the rectum, nerve bundles of various sizes interlaced irregularly with one another to form a network. However, this network was free from ganglion cells.

Acetylcholinesterase↗

PubMed2000

Presynaptic nicotinic acetylcholine receptors in the myenteric plexus of guinea pig intestine.

Presynaptic nicotinic acetylcholine receptors (nAChRs) were studied in myenteric plexus preparations from guinea pig ileum using intracellular electrophysiological methods. Microapplication of nicotine (1 mM) caused a biphasic depolarization in all AH neurons (n = 30) and in 36 of 49 S neurons. Cytisine (1 mM) caused fast depolarizations in S neurons and no response in AH neurons. Mecamylamine (10 microM) blocked all responses caused by nicotine and cytisine. TTX (0.3 microM) blocked slow excitatory synaptic potentials in S and AH neurons but had no effect on fast depolarizations caused by nicotine. Nicotine-induced slow depolarizations were reduced by TTX in two of twelve AH neurons (79% inhibition) and four of nine S neurons (90+/-12% inhibition). Slow nicotine-induced depolarizations in the remaining neurons were TTX resistant. TTX-resistant slow depolarizations were inhibited after neurokinin receptor 3 desensitization caused by senktide (0.1 microM); senktide desensitization inhibited the slow nicotine-induced depolarization by 81+/-5% and 63+/-15% in AH and S neurons, respectively. A low-calcium and high-magnesium solution blocked nicotine-induced slow depolarizations in AH neurons. In conclusion, presynaptic nAChRs mediate the release of substance P and/or neurokinin A to cause slow depolarizations of myenteric neurons.

Alkaloids↗

PubMed1984

Opioid receptor reserve in normal and morphine-tolerant guinea pig ileum myenteric plexus.

We have measured the opioid receptor reserve in the guinea pig ileum myenteric plexus by means of the site-directed alkylating agent, beta-chlornaltrexamine. Treatment of the tissue with low (less than 10 nM) concentrations of beta-chlornaltrexamine caused a parallel shift of the log concentration-response curves for both normorphine and dynorphin A-(1-13). Analysis of the resulting curves indicated that the Kd values were 1.5 +/- 0.5 X 10(-6) and 10 +/- 4 X 10(-9), respectively. Using the naloxone Ke to distinguish between the mu and kappa receptors in this tissue, we found that the receptor selectivities of normorphine and dynorphin A-(1-13) were unchanged after a maximum parallel shift, thus demonstrating that there are both spare mu and spare kappa receptors present. The spare-receptor fraction for both receptor types was about 90%. In morphine-tolerant preparations (chronic pellet implantation), there was an apparent reduction in the fraction of spare mu receptors without any change in the apparent affinity of normorphine. Reduction in the spare receptor fraction does not necessarily imply reduction in the number of binding sites. We suggest that this reduction in receptor reserve is the basis of opioid tolerance, since the agonist concentration needed to produce a given effect is expected to increase as the receptor reserve decreases.

Animals↗

PubMed2004

Loss of glia and neurons in the myenteric plexus of the aged Fischer 344 rat.

Over the normal lifespan, a subpopulation of myenteric neurons in the small and large intestines dies. This loss is one possible mechanism for the disruptions of gastrointestinal function seen in the elderly. Little, however, is known about how the glia constituting the supportive cells of the myenteric plexus may change with aging and the losses of the enteric neurons. The goal of the present study, therefore, was to determine what, if any, changes occur in the glia associated with myenteric neurons in the aged gut. Two experimental groups, consisting of adult (5-6 months of age, n = 8) or aged (26 months of age, n = 8) virgin male Fischer 344 rats, fed ad libitum, were examined. The duodenum, jejunum, ileum, colon, and rectum from each rat were prepared as whole mounts, and indirect immunofluorescence was used to visualize the myenteric glia and neurons (antibodies to S-100 and the HuC/D protein, respectively). Separate counts of glia and neurons from the same specimens were determined, and these counts were expressed both as per ganglionic area and as per ganglion to correct for "dilution" effects resulting from age-associated changes in tissue area. Significant reductions in both the numbers of glia as well as neurons occurred in every region of the small and large intestine sampled from aged rats, except for the rectum, where a nonsignificant decrease was observed. Glial loss was proportional to neuronal death, suggesting an interdependency between the two cell types. Thus, an understanding of the nature of the neuron-glia interaction in the enteric nervous system may provide insight into the deterioration of function seen in the aged gut.

Aging↗

PubMed1981

Evidence that the action of cholecystokinin octapeptide on the guinea pig ileum longitudinal muscle is mediated in part by substance P release from the myenteric plexus.

Studies were made on the mode of action of cholecystokinin octapeptide (CCK8) on longitudinal muscle strips of guinea pig ileum in vitro. CCK8 produced dose-related contractions of innervated strips of ileum longitudinal muscle (EC50 3--4 x 10(-9) M), but was inactive on denervated strips. Tetrodotoxin, and reducing the bath temperature to 15 degree C, abolished the response of innervated strips to CCK8. These results indicate that the action of CCK8 on ileal longitudinal muscle is mediated by the myenteric plexus. Atropine abolished the responses to acetylcholine and to low doses of CCK8. However, the responses to CCK8 in doses above 10(-8) M were reduced by atropine but not abolished. Incubation of longitudinal muscle strips with high concentrations of substance P (1.5 x 10(-7) M) resulted in desensitization to this peptide; this treatment inhibited the responses to CCK8 alone, and abolished the atropine-resistant actions of CCK8. Desensitization to substance P had no effect on the responses to acetylcholine, histamine, serotonin and angiotensin II. The results indicate that CCK8 contracts the longitudinal muscle of guinea pig ileum by releasing acetylcholine and substance P from the myenteric plexus.

Acetylcholine↗

PubMed1992

Induced release of acetylcholine from guinea pig ileum longitudinal muscle-myenteric plexus by anatoxin-a.

Anatoxin-a (ANTX), a nicotinic agonist, has been shown to induce contraction of guinea pig ileum, which was abrogated by the muscarinic antagonist atropine and the nicotinic antagonists tubocurarine and hexamethonium. We showed here that the ganglionic nicotinic antagonist mecamylamine was a better inhibitor of the contraction of ileum induced by ANTX. The sodium channel blocker tetrodotoxin also abolished ANTX-induced contraction. In contrast, alpha-bungarotoxin, the muscle type nicotinic receptor blocker, had no effect on ANTX-induced contraction of guinea pig ileum. Longitudinal muscle-myenteric plexus prepared from guinea pig ileum, labeled with [3H]choline and then incubated with ANTX was shown for the first time to release [3H]acetylcholine (ACh) in a dose-dependent manner. Pretreatment of longitudinal muscle-myenteric plexus with tubocurarine, hexamethonium or mecamylamine blocked ANTX-induced release of [3H]ACh. In contrast, atropine was without effect. Mecamylamine was the most potent antagonist. As observed in ileum contraction, tetrodotoxin completely and potently blocked the release of [3H]ACh induced by ANTX. Neither alpha-bungarotoxin nor the neuromuscular junction blockers conotoxin G1 or M1 could inhibit the [3H]ACh release. Taken together, these results suggested that ANTX activated nicotinic receptors on ganglionic interneurons to trigger a release of ACh, which next stimulated muscarinic receptors and induced ileum contraction.

Acetylcholine↗

PubMed1986

An inflammatory axonopathy of the myenteric plexus producing a rapidly progressive intestinal pseudoobstruction.

A previously well 39-yr-old man presented with a 4-wk history of abdominal pain, nausea, vomiting, and weight loss. An upper gastrointestinal examination showed retained food in the stomach and duodenal dilatation. A radioisotope meal showed little gastric emptying; esophageal manometry was normal. Because of persistent symptoms, a duodenojejunostomy was done. However, the patient remained symptomatic and after an episode of profuse vomiting, aspirated and died 10 wk after initial presentation. At autopsy, no tumor was found. Hematoxylin and eosin stains throughout the gastrointestinal tract showed many lymphocytes and plasma cells within the myenteric plexus. Silver stains showed the argyrophilic and argyrophobic neurons to be normal, but axons showed beading, fragmentation, and dropout in all areas. We therefore concluded the following: intestinal pseudoobstruction can be caused by an inflammatory neuropathy of the myenteric plexus, not associated with a distant carcinoma, and this process produced an axonopathy while sparing neuron bodies.

Adult↗

PubMed1997

Different effects of reducing agents on omega-conotoxin GVIA inhibition of [3H]-acetylcholine release from rat cortical slices and guinea-pig myenteric plexus.

1. The effect of reducing reagents on omega-conotoxin GVIA (omega-CgTX) inhibition of the release of [3H]-acetylcholine ([3H]-ACh) induced by tityustoxin, K+ 50 mM and electrical stimulation was investigated in rat brain cortical slices. 2. In cortical slices the inhibition of tityustoxin or electrically-stimulated [3H]-ACh release by omega-CgTX was dramatically increased by reducing reagents ascorbate or beta-mercaptoethanol. Dehydroascorbic acid did not substitute for ascorbate. 3. Depolarization induced by K+ 50 mM caused [3H]-ACh release from cortical slices which was not inhibited by omega-CgTX, even in the presence of ascorbate. 4. In the guinea-pig myenteric plexus, omega-CgTX inhibition of the tityustoxin induced release of [3H]-ACh was independent of ascorbate. 5. It is suggested that N-type-like calcium channels in guinea-pigs myenteric plexus may have pharmacological/biochemical diversity from similar channels of rat cerebral cortex.

Acetylcholine↗

PubMed1983

Morphological studies of electrophysiologically-identified myenteric plexus neurons of the guinea-pig ileum.

The morphology of neurons in the myenteric plexus of the guinea-pig ileum has been studied by means of the intracellular application of Procion Yellow. Sixty-six electrophysiologically-unidentified cells showed a great variety of soma shapes and number of processes, the vast majority of the longer of which were circumferentially-orientated. The electrophysiological properties of an additional 47 neurons were ascertained; 29 were neurons with a slow after-hyperpolarization (AH-neurons), 14 showed fast excitatory synaptic potentials (S-neurons) and 4 were of neither category. Twenty-two of the AH-neurons had a smooth soma outline and, on average, each had 5 processes, of which the great majority of long processes were circumferentially-orientated and intraganglionic. The projection ratios of oral:circumferential:aboral processes were 6:61:9. Branching was a prominent feature of the processes. In contrast, a large soma with many broad, short processes was a feature of 8 of 14 S-neurons studied. The average number of processes was 8.6 per cell and relatively more of them were aborally-directed, giving projection ratios of 2:21:7. There was, however, such a variation and overlap in the morphology of AH- and S-neurons that it was not possible to achieve a simple, reliable classification. It is concluded that many neuronal processes may be intraganglionic and that longitudinal ones are mainly aboral. From the varied morphological characteristics of AH-neurons, it is unlikely that these neurons subserve a single function in the plexus. For the same reasons S-neurons may fulfil different physiological roles.

Animals↗

PubMed1995

Plasticity in the myenteric plexus of the rat ileum after long-term sympathectomy.

To investigate the effect of chronic sympathectomy on the innervation of a tissue with an extensive intrinsic component, 1-week-old rat pups were treated with 50 mg/kg guanethidine for 3 weeks, a treatment shown to produce complete and long-lasting sympathectomy, and the ileum examined. Changes in the levels of noradrenaline, neuropeptide Y, calcitonin gene-related peptide, substance P and vasoactive intestinal polypeptide in the external muscle layers containing the myenteric plexus of the ileum were determined between 6 and 20 weeks of age. After sympathectomy, noradrenaline levels were initially depleted (3% of age-matched controls at 6 weeks, P < 0.001, and 18% of age-matched controls at 12 weeks, P < 0.001), but were not significantly reduced at 20 weeks (67% of age-matched controls). Such increases in noradrenaline content with time after sympathectomy did not occur in the mesenteric vein (levels in 20-week-old sympathectomized rats were 2% of the control values (P < 0.001). In the myenteric plexus, catecholamine fluorescent nerve fibers were seen in the 12-week-old sympathectomized rats, although tyrosine hydroxylase-immunoreactivity was absent. Guanethidine sympathectomy had no effect on the neuropeptide levels in 6-week-old rat ileum but there was a selective increase at 20 weeks; the levels of calcitonin gene-related peptide and substance P were increased (X3, P < 0.001 and X1.6, P < 0.05, respectively) while vasoactive intestinal polypeptide and neuropeptide Y levels were unchanged. Short-term sympathectomy (destruction of sympathetic nerve terminals by acute 6-hydroxydopamine treatment) had no affect on noradrenaline or peptide levels in this tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗

PubMed1997

Ultrastructural relationships of spinal primary afferent fibres with neuronal and non-neuronal cells in the myenteric plexus of the cat oesophago-gastric junction.

Spinal primary afferent fibres innervating the myenteric area in the oesophago-gastric junction of the cat were selectively labelled by anterogradely transported cholera toxin B subunit-horseradish peroxidase conjugate injected into thoracic dorsal root ganglia. The ultrastructure of these labelled primary afferent fibres was studied in order to determine whether they display close relationships with specific cell types in the myenteric plexus. Horseradish peroxidase was revealed with tetramethylbenzidine stabilized with ammonium heptamolybdate or with the tetramethylbenzidine/tungstate reaction in order to visualize the cytoplasmic organelles and the axolemma, respectively. The labelled primary afferent fibres were unmyelinated. Two kinds of profiles of labelled fibres containing vesicles and mitochondrial accumulations were found: (i) fibres running in myenteric connectives in isolated nerve bundles, and (ii) fibres within the myenteric ganglia. The first kind had small areas of axolemma with no glial cell covering, whereas the second kind had little or no glial cell covering (termed naked primary afferent fibres). In addition, labelled fibres containing few vesicles and mitochondria and running in nerve bundles surrounded by perineurium were numerous. Within the myenteric ganglia, naked primary afferent fibres contacted myenteric neurons. The contacts were mainly axosomatic. No synaptic specializations were distinguished. In the interganglionic area, some labelled fibres terminated close to blood vessels. The intraganglionic naked primary afferent fibres are suggested to be mechanoreceptors. Their exposed axolemma might allow both mechanotransduction and release of neurotransmitters which could act on myenteric neurons. Because they are protected by their glial cell sheath and by bundles of collagen fibrils, interganglionic primary afferent fibres are likely to be less exposed to deformation.

Afferent Pathways↗

PubMed1965

SEROTONIN: SYNTHESIS AND RELEASE FROM THE MYENTERIC PLEXUS OF THE MOUSE INTESTINE.

After injection of its radioactive precursor, 5-hydroxytryptophan, radioactive serotonin was biosynthesized and bound in the myenteric plexus of the mouse intestine. Addition of nonradioactive serotonin to preparations in vitro caused a net release of radioactive serotonin from the plexus. This release appeared to result from activity in the intramural nervous system of the intestine. A neurotransmitter role between sensory and motor neurons in the peristaltic reflex pathway is suggested as a working hypothesis to explain the action of serotonin.

5-Hydroxytryptophan↗