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PubMed1991

Nonspecific tolerance in ileal circular muscle-myenteric plexus preparations from morphine-pretreated guinea pigs.

Guinea pigs were treated for 6 to 8 days by s.c. implantation of pellets, each containing a mixture of morphine base (120 mg) and morphine hydrochloride (35 mg). Each guinea pig received one pellet. Circular muscle-myenteric plexus preparations from the pretreated animals exhibited 6.1-fold tolerance to the inhibitory effects of morphine on nerve-mediated contractions of the circular muscle. Morphine-tolerant tissues were also tolerant to the inhibitory effects of another mu agonist, (D-Ala2-N-Me-Phe4,Gly5- ol)enkephalin (2.7-fold), the selective kappa agonist, dynorphin (4.0-fold), the adrenoceptor agonist, clonidine (22-fold) and the adenosine receptor agonist, 2-chloroadenosine (43-fold). That is, tissues were tolerant to four inhibitory agents that acted via four distinct receptors. Tolerance therefore cannot be explained by a change in the opioid receptor that was occupied chronically by morphine. Nonspecific tolerance would result if an intracellular effector mechanism that was shared by each agonist was altered by morphine pellet implantation. Alternatively, tolerance could be a consequence of the neuronal hyperexcitability that is induced by chronic exposure to morphine. As such, inhibitory agents, irrespective of the receptors or intracellular mechanisms that they activate, may be less effective in reducing the excitability of myenteric neurons and hence less effective in decreasing transmitter release.

2-Chloroadenosine↗

PubMed1990

Dextrorphan binds to opioid receptors in guinea-pig brain membranes and is an antagonist at opioid receptors in myenteric plexus.

Dextrorphan (+)-tartrate, purified by repeated crystallization to remove all traces of the enantiomer levorphanol, binds to mu, delta, and kappa sites on guinea-pig brain membranes with lower affinities (by a factor of 400-3200) than levorphanol. In the guinea-pig ileum myenteric plexus longitudinal muscle preparation (GPI), dextrorphan, at 100-200 microM, inhibits the electrically stimulated twitch, but this action is not blocked or reversed by naloxone; both (+)- and (-)-naloxone produce similar non-opioid twitch inhibition at comparable concentrations. At 10-20 microM, dextrorphan blocks and reverses the twitch inhibition due to mu and kappa agonists, but the blockade can be overcome only partially by increasing the agonist concentration. We conclude that dextrorphan is an opioid ligand with low affinity and with antagonist effect on opioid receptors in the GPI.

Animals↗

PubMed1980

Structure of the myenteric plexus in the sphincters of cat gastro-intestinal tract.. II. Changes in the quantitative characteristics of the types of dense-core vesicles after reserpine treatment.

In order to elucidate the functional significance of the populations of dense-core vesicles in the myenteric plexus of the sphincters of cat gastro-intestinal tract, studies are made of the changes in their spatial density after reserpine treatment, since the action of reserpine on a definte transmitter-noradrenaline-is known. The different character and intensity of the changes in the density of the different populations of dense-core vesicles probably indicates participation in the metabolism of different transmitter systems. The lack of statistically significant changes in the number of large dense-core vesicles correlates well with the character of the relaxation upon electrical stimulation of the sphincters and suggests participation of these vesicles in the nonadrenergic noncholinergic innervation.

Animals↗

PubMed1993

Prostaglandin E2 stimulation of acetylcholine release from guinea pig myenteric plexus neurons.

Prostaglandins are widely distributed within the gastrointestinal tract and have important effects on gastrointestinal motility. Although actions upon gastrointestinal smooth muscle have been demonstrated for prostaglandins (PG), neural mechanisms may also be important. The effects of PGE2 on acetylcholine (ACh) release were studied using guinea pig myenteric plexus neurons in primary culture. PGE stimulated the release of ACh in a dose-dependent manner, with a median effective dose (ED50) of 0.8 x 10(-6) M. Involvement of L-type calcium channels was implied by the sensitivity of PGE2-stimulated ACh release to omega conotoxin or diltiazem. In addition, ACh release stimulated by PGE2 could be inhibited by co-incubation with dideoxyadenosine or Rp-cAMPS, agents that act upon cyclic adenosine monophosphate (cAMP)-dependent signaling pathways. PGE2 has direct effects upon myenteric neurons to stimulate cholinergic transmission.

Acetylcholine↗

PubMed2001

Effect of 1DMe, a neuropeptide FF analog, on acetylcholine release from myenteric plexus of guinea pig ileum.

Since neuropeptide FF (NPFF) is a putative neurotransmitter to exert anti-opioid activity, we examined the effects of [D-Tyr', (NMe)Phe3]neuropeptide FF (IDMe), a stable NPFF analog, on acetylcholine (ACh) release from a longitudinal muscle-myenteric plexus (LMMP) preparation of guinea pig ileum in which opioids were known to inhibit ACh release when muscarinic autoinhibition was not fully activated. In the presence of atropine, 1DMe increased spontaneous and electrical field stimulation (EFS)-evoked ACh release in a concentration-dependent manner. Naloxone also increased ACh release. The stimulatory effects of 1DMe and naloxone were not additive. In the absence of atropine, 1DMe did not affect ACh release. Morphine decreased spontaneous and EFS-evoked ACh release in the presence of 1 microM atropine. 1DMe as well as naloxone counteracted the inhibitory effects of morphine on EFS-evoked ACh release. The combination of 1DMe and naloxone was not more inhibitory than either drug alone. 1DMe had no appreciable effect on norepinephrine-induced inhibition of spontaneous and EFS-evoked ACh release. These results first demonstrated the effects of a NPFF analog on neurotransmitter release: 1DMe had a stimulatory effect on spontaneous and EFS-induced ACh release from the LMMP preparation of guinea pig ileum, probably by counteracting the inhibitory effect of endogenous opioids on ACh release.

Acetylcholine↗

PubMedDate not supplied

Myenteric plexus in spastic motility disorders.

Previous studies have often revealed an absence or reduction of ganglia in Auerbach's plexus in many patients with achalasia, which has been postulated to be related to the elevated lower esophageal sphincter pressure in these patients. We undertook a prospective study to determine whether microscopic changes were present in the myenteric plexus of patients with hypertensive lower esophageal sphincter, nutcracker esophagus, and diffuse esophageal spasm and if there was a correlation with lower esophageal sphincter pressure. Nine patients (3 men and 6 women; ages 49 to 72 years, mean 58 years) underwent a laparoscopic esophagomyotomy with fundoplication for symptomatic spastic motility disorder. A 10 mm x 5 mm segment of esophageal muscle was removed from the border of the myotomy incision, fixed in formalin, and examined under light microscopy for the presence or absence of ganglia and inflammation. Correlation between the presence of ganglia and lower esophageal sphincter pressure was tested by Pearson's bivariant correlation. Manometry revealed three patients with hypertensive lower esophageal sphincter, four patients with nutcracker esophagus, and two patients with diffuse esophageal spasm. All three patients with a hypertensive lower esophageal sphincter revealed an absence of ganglia, whereas the six patients with nutcracker esophagus and diffuse esophageal spasm exhibited ganglia despite an elevated lower esophageal sphincter pressure in four. Hypertensive lower esophageal sphincter resembled achalasia in its absence of ganglia in Auerbach's plexus, whereas nutcracker esophagus and diffuse esophageal spasm exhibited ganglia. There was no significant correlation in our series between the presence of ganglia and an elevated lower esophageal sphincter pressure in spastic motility disorders.

Esophageal Motility Disorders↗

PubMed1998

Inhibitory effect of endomorphin-1 and -2 on acetylcholine release from myenteric plexus of guinea pig ileum.

Endomorphin-1 and -2, putative endogenous ligands for the mu-opioid receptor, inhibited acetylcholine (ACh) release evoked by electrical field stimulation (EFS) at 1 Hz, which partially activates muscarinic autoreceptors, but not at 10 Hz, which fully activates muscarinic autoreceptors, in longitudinal muscle with the myenteric plexus (LMMP) preparations of guinea pig ileum. After blockade of autoinhibition by atropine, the peptides also inhibited EFS-evoked ACh release at 10 Hz. The inhibitory effects on ACh release were abolished by the mu-opioid antagonist cyprodime. These results suggest that endomorphin-1 and -2 inhibit ACh release from LMMP preparations of guinea pig ileum and that the mechanism of the inhibition must have a component in common with muscarinic autoinhibition.

Acetylcholine↗

PubMed1990

Evidence that the agonist action of dynorphin A(1-8) in the guinea-pig myenteric-plexus may be mediated partly through conversion to [Leu5]enkephalin.

1. The agonist action of the opioid peptide dynorphin A(1-8) on the myenteric plexus-longitudinal muscle of the guinea-pig ileum has been characterized. 2. The endogenous opioid peptide dynorphin A(1-8) was rapidly degraded by slices of myenteric plexus-longitudinal muscle of the guinea-pig ileum. 3. A product of the degradation was the delta-receptor preferring [Leu5]enkephalin. Levels of [Leu5]enkephalin were markedly increased in the presence of the peptidase inhibitors bestatin, thiorphan and captopril. 4. In the myenteric plexus dynorphin A(1-8) acted as a kappa-receptor agonist. In the presence of bestatin, thiorphan and captopril a mu-receptor agonist effect was observed. This mu-agonist action was lost in the presence of N-[1-(RS)-carboxy-2-phenylethyl]Ala-Ala-Phe-p-aminobenzoate, an inhibitor of the endopeptidase enzyme EC 3.4.24.15. 5. The results suggest that formation of [Leu5]enkephalin from dynorphin A(1-8) may be an important conversion process. The enzyme responsible may be the Zn2(+)-metalloendopeptidase, EC 3.4.24.15.

Animals↗

PubMed1992

Neuronal and myogenic muscarinic effects of McN-A-343 on guinea pig longitudinal smooth muscle-myenteric plexus.

Among muscarinic agonists, the compound McN-A-343, originally proposed as selective stimulant of M1 cholinergic site, was subsequently questioned as a useful pharmacological tool in the classification of muscarinic receptors. In this work, evidence is presented for a dual response of McN-A-343 on longitudinal muscle-myenteric plexus preparation. On electrically-stimulated preparation, this agonist exhibited a pirenzepine-sensitive inhibition of the twitch contractions due to the involvement of neural M1-muscarinic receptor. On the other hand, a direct myogenic contractile action on the unstimulated tissue was observed using McN-A-343 in the same range of concentrations. This latter response, on the basis of the effects of muscarinic and non-muscarinic antagonists tested, seems to involve effectorial muscarinic sites with an unusual mechanism.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

PubMed1998

Some neurohistochemical properties of nerve elements in myenteric plexus of rabbit ileum: similarities and dissimilarities to the rodent pattern.

Enteric neurons have distinct neurochemical codings in each species. The basal tone of the gastrointestinal tract of the rabbit is low and produces neurally evoked pendular movements. Therefore, it might have an innervation pattern different from that of other laboratory animals. We have characterised myenteric neuron populations in rabbit ileum with neurochemical markers that are known to be associated with distinct cell types and/or fibre systems in the myenteric plexus. The density of nerve cells estimated with the NADH-diaphorase technique was about 2500 cells/cm2 and most, if not all, neurons contained microtubule-associated protein 2. NADPH-diaphorase-positive cells were numerous. One cell type was large and emitted long straight processes, whereas small cells bore thin filamentous dendrites. Neurons immunoreactive for 28-kDa calcium-binding protein were rare. Over 70% of them had very strongly labelled lamellar dendrites. Their axons were beaded and formed pericellular baskets around unstained somata. We found very few small tyrosine-hydroxylase-positive cells. The fibre network in the plexus was very strong; the axons formed many pericellular baskets. In double labelling studies, no co-localisation was revealed between the 28-kDa calcium-binding protein and NADPH-diaphorase. Some fibres containing 28-kDa calcium-binding protein formed only a few contacts on somata of NADPH-diaphorase-positive cells. None of the NADPH-diaphorase-labelled cells were found to be stained for tyrosine hydroxylase. Tyrosine-hydroxylase-positive fibres rarely made pericellular baskets on the surface of NADPH-diaphorase-positive somata. Strongly immunolabelled pericellular baskets were never observed around NADPH-diaphorase-positive cell somata. The results suggest that myenteric neurons in rabbit comprise distinct and characteristic neurochemical properties that are different from the rodent pattern. Therefore, the explanation of the motility pattern of rabbit intestine can be approached on a chemical neuroanatomical basis.

Animals↗

PubMed1985

Dynorphin-A(1-8) and gamma-melanotropin exist within different myenteric plexus neurons of rat duodenum.

Using the adjacent serial section staining technique and the double staining elution method, it was demonstrated that the opioid peptide dynorphin-A(1-8), originating from the prodynorphin precursor, and gamma 3-melanotropin (gamma 3-MSH), originating from the pro-opiomelanocortin (POMC) precursor, did not co-exist within myenteric plexus perikarya of the rat duodenum. This finding resembles that of the rat brain. Whether gamma 3 -MSH and dynorphin-A(1-8) act synergistically or antagonize each other in some physiological functions or have no interaction at all in the rat duodenum is as yet unknown.

Animals↗

PubMed1990

Auerbach's myenteric plexus. A possible site of origin for gastrointestinal stromal tumors in von Recklinghausen's neurofibromatosis.

We present a case of multiple benign spindle cell tumors of the jejunum in a patient with von Recklinghausen's neurofibromatosis and describe the light-microscopic, immunohistochemical, and ultrastructural features of these lesions. Two small spindle cell nodules were located in the region of Auerbach's myenteric plexus and a third larger tumor produced a subserosal mass. The immunohistochemical profile of these tumors revealed that they were actin and S100-protein negative but positive for neuron-specific enolase. At the ultrastructural level, the tumors recapitulated features of Auerbach's plexus. These lesions are similar to previously described gastrointestinal autonomic nerve tumors, and we propose that this may be the site of origin of enteric stromal tumors in von Recklinghausen's neurofibromatosis.

Carcinoma↗

PubMed1996

Morphological changes in the myenteric plexus of rat ileum after transection and end-to-end anastomosis.

Surgical interruption of the gastrointestinal tract is widely used for investigating the structure of the enteric nervous system and in the treatment of certain pathological conditions of the gastrointestinal tract. The effects of transection and end-to-end anastomosis and myotomy on nerve cells of the myenteric plexus were studied by light and electron microscopy, 1, 2 and 6 wk postsurgically. During the 1st wk, degeneration of some nerve cells was indicated by the dilation of the endoplasmic reticulum and dispersion of Nissl substance. The degenerative process (an early electron-dense lamellar degeneration and a late floccular degeneration) was accompanied by some regenerative changes during the recovery period. Quantitative light microscopic analysis demonstrated a significant decrease in the number of neurons located 1 and 5 mm from operation sites in the intestine.

Anastomosis, Surgical↗

PubMed1994

Transplantation of the postnatal rat myenteric plexus into the adult rat corpus striatum: an electron microscopic study.

Since the enteric nervous system (ENS) has been demonstrated to display many similarities with the central nervous system (CNS), we have undertaken investigations examining the possibility of using the ENS as a source of neurons for transplantation into the brain in neurodegenerative diseases. Grafts of freshly dissected myenteric plexus taken from young inbred Fischer rats were implanted in the corpus striatum of adult Fischer rats, some of which had received a quinolinic acid lesion 1 to 2 weeks prior to implantation. Brain sections from the grafted animals were examined electron microscopically 3 and 6 weeks after implantation. Grafts contained many enteric neurons and glial cells in ganglia morphologically similar to those seen within the intestine. Although a glia limitans could be observed in parts of the interface between graft and brain, ganglia at the surface of the graft were observed to be closely apposed to the surrounding striatum, with no intervening basal lamina. CNS axonal sprouts were identified in the corpus striatum near the interface with the grafted enteric ganglia and bundles of similar axons, some containing fibers that had enlarged and become myelinated, could be seen within the grafts. A smaller number of CNS axonal sprouts were also observed around the grafts in the quinolinic-acid-lesioned striata. This study confirms that even in the absence of surrounding layers of smooth muscle, enteric ganglia grafted into the corpus striatum survive and stimulate the production of axonal sprouts from striatal and other neurons, which subsequently grow into the grafts.

Animals↗

PubMed1986

Inhibitory peptidergic neurons: functional difference between somatostatin and enkephalin in myenteric plexus.

This study reports on a difference in the inhibitory action of the neuropeptides somatostatin and Met-enkephalin on acetylcholine (ACh) release from myenteric plexus-longitudinal muscle strips of guinea pig small intestine. Met-enkephalin (8.7 X 10(-8) M) inhibited ACh release evoked by either substance P (3.7 X 10(-8) M) or neurotensin (7.5 X 10(-11) M), and this inhibition could be reversed by naloxone (5 X 10(-8) to 5 X 10(-5) M). Neurotensin-induced ACh release was also sensitive to the inhibition by somatostatin. However, when tested in a dose range from 6.1 X 10(-8) to 6.1 X 10(-6) M, somatostatin was ineffective in reducing the efflux of ACh evoked by substance P. These observations provided evidence to support the view that inhibitory peptidergic neurons within the myenteric plexus modulate the activity of cholinergic neurons with a high degree of specificity and that both somatostatin and Met-enkephalin have distinct neuromodulatory functions in the gut.

Acetylcholine↗

PubMed1988

[Distribution of fibronectin and laminin during development of the human myenteric plexus and Hirschsprung's disease].

The distribution of fibronectin and laminin, two glycoproteins involved in the migration of neural crest cells, was studied by an indirect immunohistofluorescence technique in 35 embryos and fetuses (from 6 weeks old to birth), 5 normal controls, and 6 patients with Hirschsprung's disease, in order to provide a new approach to the embryogenesis of human myenteric plexus and the pathogenesis of aganglionosis. Fibronectin was not seen near individual neuroblasts unlike myoblasts and mesenchymal cells which were surrounded by this macromolecule. There was a progressive and parallel cephalocaudal development of the plexus and the muscular layers from the esophagus to the intestine. However, in the rectum, at 7 weeks, neuroblasts were detected in close contact to fibronectin-labeled cells whereas they were not in the colon. These present results were in favor of two origins for neuroblasts: the vagal and the caudal neural crest cells. Faulty migration of caudal neural crest cells might be involved in the aganglionosis of Hirschsprung's disease in spite of the fact that local environment of fibronectin and laminin was identical to that of normal subjects.

Adult↗

PubMed1989

Glutamate receptors of the N-methyl-D-aspartate subtype in the myenteric plexus of the guinea pig ileum.

The excitatory amino acids L-glutamate and N-methyl-D-aspartate (NMDA) produced contractions of the myenteric plexus-longitudinal muscle preparation of the guinea pig ileum over the concentration range of 3 X 10(-6) to 10(-3) M. The contractile response to L-glutamate and NMDA, but not carbamyl choline, was blocked noncompetitively by 0.6 mM Mg++. In the absence of Mg++, concentration-dependent increases in contractile force also were produced by, in order of potency, L-aspartate, L-homocysteate and D-glutamate, but not by quisqualate, kainate or quinolinate. L-Glutamate was competitively antagonized by the selective NMDA receptor antagonists D-2-amino-5-phosphonovalerate and 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (3 X 10(-6)-3 X 10(-5) M), as well as by the nonselective excitatory amino acid antagonist gamma-D-glutamylglycine (3 X 10(-4) M). Glutamic acid diethyl ester (3 X 10(-4) M) noncompetitively antagonized L-glutamate. L-Glutamate was not blocked by gamma-D-glutamylaminomethyl sulphonate (3 X 10(-4) M), an antagonist which preferentially antagonizes kainate and quisqualate. In addition, the phencyclidine-like drugs etoxadrol (10(-7)-10(-5) M), dextromethorphan (10(-6)-10(-5) M) and 5-methyl-10,11-dihydroxy-5H-dibenzo(a,d)cyclohepten-5,10-imine (10(-9)-10(-7) M) noncompetitively antagonized L-glutamate. The (+) isomer of 5-methyl-10, 11-dihydroxy-5H-dibenzo(a,d)cyclohepten-5,10-imine was approximately 10-fold more potent than the (-) isomer in antagonizing L-glutamate. The present results demonstrate that receptors for the excitatory amino acid L-glutamate are present in the guinea pig myenteric plexus and are of the NMDA subtype.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1977

Antidiarrheal and central nervous system activities of SC-27166 (2-[3 - 5 - methyl - 1, 3, 4 - oxadiazol - 2 - yl) - 3, 3 - diphenylpropyl] - 2 - azabicyclo [2.2.2]octane), a new antidiarrheal agent, resulting from binding to opiate receptor sites of brain and myenteric plexus.

Pharmacological studies were performed to investigate the interaction of SC-27166 (2-[3-(5-methyl-1,3,4--oxadiazol-2-yl)-3,3-diphenylpropyl]-2-azabicyclo[2.2.2]octane), a new antidiarrheal agent, with opiate receptor sites in vitro and in vivo. Morphine, loperamide and SC-27166 inhibited the binding of [3H]naloxone to homogenates of guinea-pig brain and myenteric plexus and the inhibition was diminished in the presence of 100 mM Na+. Unlike that of morphine and [3H]naloxone itself, the binding of loperamide and SC-27166 was complex and Scatchard plots indicated the presence of low and high affinity sites for both compounds. Morphine, loperamide and SC-27166 inhibited the contractions of electrically driven longitudinal muscle from guinea-pig ileum and naloxone antagonized these effects. In the anesthetized dog, i.v. administration of morphine and SC-27166 enhanced the contractile activity of circular muscle in proximal and distal duodenum and distal ileum but duodenal longitudinal muscle was relaxed; these effects were completely reversed by subsequent administration of naloxone. In the rat, p.o. administration of loperamide and SC-27166 inhibited intestinal propulsion at doses considerably lower than were necessary to produce activity in the hot plate test; this specificity of action was not seen with morphine. In the rat, p.o. administration of loperamide and SC-27166 inhibited diarrhea at doses considerably lower than were necessary to produce withdrawal symptoms. The authors concluded that both loperamide and SC-27166 are specific antidiarrheal agents that produce both their central and antidiarrheal effects by binding to opiate receptor sites.

Animals↗