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PubMed1987

[Theophylline-induced changes in the presynaptic effects of adenosine, baclofen, clofelin and morphine in the myenteric plexus of the guinea pig].

The experiments on the isolated guinea-pig ileum have shown that the contractions caused by low frequency transmural stimulation are decreased by adenosine, baclofen, clofelin and morphine. Theophylline is a competing antagonist of adenosine and a noncompeting antagonist of baclofen, clofelin and morphine. The effects of the latter are not altered by 1,3-dipropyl-8-phenylxanthine suppressing adenosine effects. It is concluded that presynaptic effects of baclofen, clofelin and morphine depend on cAMP level in cholinergic neurons of myenteric plexus.

Adenosine↗

PubMed1996

Histochemical evidence of the increased expression of nicotinamide adenine dinucleotide phosphate-dependent diaphorase in neurons of the myenteric plexus after acute spinal cord injury in adult rats.

The expression of nitric oxide synthase in neurons of the gastrointestinal tract (GIT) after experimental spinal cord injury (SCI) was assessed in adult rats contused at T8. One day and 10 weeks after injury, specimens along the GIT were studied for NADPH-diaphorase histochemistry. A significant increase in the number of positive cell bodies and fibers in the myenteric plexus were observed 1 day after SCI, as compared to specimens from control and chronically injured rats, with the exception of the colon, which showed unchanged or decreased number of positive neurons in the acute and chronic stages, respectively. Positive neurons in the submucous plexus remained unchanged, excepting an increase in the colon after acute SCI, and a decrease in the duodenum in chronically injured rats. The altered nitric oxide neurotransmission in the GIT may be relevant to its reduced motility after SCI.

Acute Disease↗

PubMed2002

Effects of extrinsic autonomic denervation and myenteric plexus transection on colonic motility in conscious dogs.

BACKGROUND: The role of extrinsic autonomic nerves in regulation of colonic contractile activity is not well understood. METHODS: Twelve dogs had 6 strain gauge force transducers implanted in the colon and were divided into 3 experimental groups: (1) a control group, (2) an extrinsic denervation group (denervation group), and (3) an extrinsic denervation with proximal intrinsic myenteric plexus transection group (denervation + transection group). After recovery, colonic contractile activity during fasting and effects of feeding on gastrocolonic response were recorded. RESULTS: Colonic contractile activity occurred not only in the denervation group but also in the denervation + transection group. Both mean duration and propagation time of the colonic contractile activity were shorter in the denervation + transection group than in the control group. In the denervation group, propagation time was shorter than in the controls but the other parameters were not different. Feeding failed to immediately induce the gastrocolonic response in both experimental groups. CONCLUSIONS: We conclude that extrinsic nerves are not required for the appearance of colonic contractile activity. However, colonic contractile activity and its propagation are modulated by extrinsic innervation or proximal intrinsic neural continuity. Gastrocolonic response may be predominantly under extrinsic neural control.

Animals↗

PubMed1994

Inhibition of cholinergic transmission by opiates in ileal myenteric plexus is mediated by kappa receptor. Involvement of regulatory inhibitory G protein and calcium N-channels.

Opiates are known to influence intestinal motility via modulation of cholinergic transmission. The aims of this study are to characterize the opioid receptor subtype that modulates cholinergic transmission and to investigate the intracellular mechanism responsible for inhibition of acetylcholine (ACh) release by opiates using longitudinal muscle-myenteric plexus preparations of the guinea pig ileum. The kappa-receptor agonist U50488H and the mu-receptors agonist [D-Ala2,N-Me-Phe4, Gly5-ol]enkephalin, inhibited the release of ACh evoked by electrical stimulation (0.2 and 2 Hz) in a dose-dependent fashion, whereas the delta-receptor agonist DPDPE, had no effect. ACh release evoked by depolarization with veratridine, which was more analogous to high frequency stimulation, was inhibited only by U50488H. Pertussis toxin abolished the inhibitory effect of U50488H on veratridine-induced ACh release suggesting that the principal mechanism by which opiates inhibit cholinergic transmission is via activation of an inhibitory regulatory G protein. Veratridine-stimulated release of ACh was antagonized by omega-Conotoxin GVIA (a preferential N channel blocker) but was not affected by nifedipine (an L channel blocker) or nickel (a T channel blocker). U50488H did not produce further inhibition of veratridine-evoked ACh release in the presence of omega-Conotoxin GVIA. These results suggest that both kappa- and mu-agonists can modulate cholinergic transmission, although the kappa-agonist appears to be more potent. The kappa receptors modulate ACh release by inhibition of N-type voltage-sensitive Ca++ channels via a pertussis toxin-sensitive G protein in guinea pig ileum.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1987

Chemical denervation of the myenteric plexus of the muscular stomach of turkeys.

1. The thin caudoventral muscle (TCM) of the muscular stomach of domestic turkeys was surgically exposed and painted with solutions of saline or 0.1, 0.25, 0.5, and 1.0% benzalkonium chloride (BC), a cationic surfactant shown to irreversibly damage neurons but not muscle tissue in mammals. 2. Following fluoroscopic observations of gastric motility for 2 weeks, turkeys were euthanized, the entire muscular stomach was excised and weighed, and serial frozen sections of the TCM were taken for evaluation of the number and size of neurons in the myenteric plexus. 3. Treatment with 0.5 and 1.0% BC resulted in loss of motility in the TCM, significant hypertrophy (P less than 0.001) of the CTM, a 70% decrease in number and 60% decrease in size of myenteric neurons, and a 4-fold increase in thickness of the serosa, compared with saline-treated controls.

Animals↗

PubMed2005

Glutamate stimulation of acetylcholine release from myenteric plexus is mediated by endogenous nitric oxide.

Glutamate was found to be an excitatory neurotransmitter in the enteric nervous system. Although several lines of evidence indicate a role of glutamate in the regulation of gut motility and secretion the physiological significance of glutamatergic transmission is not clear yet. We studied the effect of glutamate on [3H]acetylcholine release and nicotinamide adenine dinucleotide phosphate-diaphorase staining in longitudinal muscle strips with attached myenteric plexus of guinea pig ileum. L-glutamate (100 microM) significantly enhanced both the evoked [3H]acetylcholine release and the optical density of nicotinamide adenine dinucleotide phosphate-diaphorase positive neurones, i.e. the intensity of staining. The non-competitive N-methyl-D-aspartate receptor antagonist MK-801 (3 microM) abolished the stimulatory effect of L-glutamate on acetylcholine efflux. Similarly, the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine (100 microM) significantly reduced the effect of L-glutamate on [3H]acetylcholine release and nicotinamide adenine dinucleotide phosphate-diaphorase staining. Our data suggest that endogenous nitric oxide seems to mediate the stimulatory effect of glutamate on acetylcholine release from guinea pig myenteric neurons.

Acetylcholine↗

PubMed1987

Immunocytochemical localization of GABA in cat myenteric plexus.

Transverse sections through various levels of the feline gastrointestinal tract (antrum pyloricum, duodenum, jejunum, ileum and colon) were obtained from animals perfused with a mixture of glutaraldehyde and paraformaldehyde, and incubated with an antiserum specific for glutaraldehyde-fixed GABA. This antiserum has previously been characterized and shown to react selectively with presumed GABAergic neurons in the CNS. At all levels of the gastrointestinal tract, staining was observed in varicose fibers in the myenteric plexus and the circular muscle layer. Staining was abolished by glutaraldehyde complexes of GABA previously added to the antiserum, but not by similar complexes of related amino acids. The findings strongly suggest that GABA is concentrated in a subpopulation of gastrointestinal nerve fibers and add to previous evidence favoring a transmitter role for GABA in the enteric nervous system.

Animals↗

PubMed1986

Three-dimensional organization and topographical features of the myenteric plexus (Auerbach) in the porcine small intestine: scanning electron microscopy after enzymatic digestion and HCl-hydrolysis.

The present scanning electron microscopical (SEM) study was initiated to visualize the surface topography of Auerbach's plexus in the ileum of the pig. After enzymatic digestion of the connective-tissue components of the tunica muscularis and the tunica serosa followed by glutaraldehyde fixation, HCl-hydrolysis and stripping off either the longitudinal or circular smooth muscle layer, the three-dimensional architecture and topographical features of the myenteric plexus can clearly be observed. In this way, ganglia, primary, secondary and tertiary strands, and single nerve fibres can be demonstrated. Individual nerve cells, which are incompletely covered by glial cells and by remnants of the basal lamina, can be recognized in the centre and periphery of the ganglia and adjacent to primary and secondary nerve strands.

Animals↗

PubMed2004

Spatial pattern analysis of nitrergic neurons in the developing myenteric plexus of the human fetal intestine.

BACKGROUND: Enteric nervous system precursors derived from the neural crest migrate along defined pathways to colonize the bowel. The individual cells in different environments experience different growth, differentiation, and survival conditions. Hence, the spatial distribution of the neurons is determinant with regard to functional maturation. The question arises as to whether the distribution is random or nonrandom. METHODS: Nitrergic cells were visualized by means of nicotinamide adenine dinucleotide phosphate diaphorase histochemistry. Stained specimens were photographed, and the borders of the myenteric plexus and the nuclei of the nitrergic neurons were digitalized. Plexus Pattern Analysis software was used to count the nuclei of nitrergic neurons, calculate the proportions of the areas covered by the plexus and the gut wall, and perform randomization analyses. RESULTS: The distribution pattern of the nitrergic neurons changed markedly between weeks 14 and 22 of gestation. The nitrergic neurons were randomly distributed at week 14 but were aggregated in the plexus and within the individual ganglia at week 19. The dynamics of these changes exhibited regional differences. CONCLUSIONS: The results suggest that, in addition to the gut wall and the plexus, other intraganglionic constituents may contribute to the aggregation of nitrergic cells and such examinations should be extended to other cell types in the future.

Female↗

PubMed1997

A monoclonal antibody to astrocytes, subepithelial fibroblasts of small intestinal villi and interstitial cells of the myenteric plexus layer.

A monoclonal antibody was developed, using cultured subepithelial fibroblasts of rat duodenal villi as the antigenic material, by in vitro immunization. Hybridomas were selected on cryosections of rat brain and small intestine using indirect immunofluorescence techniques. The monoclonal antibody, termed 8E1, was very useful to label GFAP-positive astrocytes in the adult rat brain, subepithelial fibroblasts of intestinal villi and Thuneberg's fibroblast-like interstitial cells associated with the myenteric plexus layer. These cells are known to be stellate in shape, forming a cellular network with extended cell processes that communicate via gap junctions. Immature astrocytes such as radial fibers were not immunolabeled with mAb-8E1. Immunoelectron microscopy revealed clustered gold labeling of 8E1 antigen on the intermediate filaments of cultured astrocytes and cultured subepithelial fibroblasts. This staining pattern was different from the continuous and linear gold labeling of GFAP and vimentin. MAb-8E1 did not immunoblot purified human brain GFAP nor bovine lens vimentin, and so was not neutralized by preabsorption with these molecules. Immunoblot analysis after SDS-PAGE showed that the antigen recognized by mAb-8E1 was a Mr 50K protein in the rat cerebra, and a Mr 56K protein in the cultured subepithelial fibroblasts. This study showed that astrocytes and some types of stellate cells share distinct antigenic properties in the components of their intermediate filaments.

Animals↗

PubMed1977

Giant axonal neuropathy. Involvement of peripheral nerve, myenteric plexus and extra-neuronal area.

A case of giant axonal neuropathy in a 8 years old child is reported by light and electron microscopy. Clinically, this case is strikingly similar to the rare previous reports and characterized by a distal neuropathy, CNS symptoms and tightly curled hair. Giant axons were found in the sural nerve but had been absent at the onset of the illness. An increase in the number of neurofilaments was found in the axons and neurons of the myenteric plexus. The number of microfilaments was also increased in various types of cells namely Schwann and endothelial cells and fibroblasts: This suggests that the metabolic disorder, probably inborn and genetic, does not only affect the nervous system.

Axons↗

PubMed1974

Two types of neurones in the myenteric plexus of duodenum in the guinea-pig.

1. Intracellular recordings have been made from neurones lying in the myenteric plexus of guinea-pig duodenum; some aspects of their membrane properties have been studied by passing current through the intracellular electrode while recording changes in membrane potential.2. The current-voltage relationship was linear for small changes in membrane potential, input resistances ranging from 125 to 250 MOmega. Larger hyperpolarizing currents (causing changes of 20-40 mV) caused the input resistance to fall.3. Depolarizing currents of 1 to 10 x 10(-10) A initiated action potentials with amplitudes of up to 95 mV.4. Two types of cell were distinguished when an action potential was initiated. In one group the action potential and undershoot had a form similar to that recorded from other mammalian ganglia. In the second group an action potential was followed by both an undershoot and a prolonged afterhyperpolarization which was associated with a decrease in cell resistance.5. The two groups of cells were further distinguished by their responses to transmural stimulation. Only those cells which did not show an afterhyperpolarization could be shown to receive a synaptic input.6. The mechanism by which each cell type generates an action potential was different. The action potentials recorded from cells which had a detectable synaptic input were abolished by tetrodotoxin. In contrast, those recorded from the other type of cells persisted in the presence of tetrodotoxin. Preliminary experiments suggest that during an action potential these cells become permeable to both sodium and calcium ions.7. Abolition of the calcium component of the action potential in cells which generated an afterhyperpolarization abolished this latter potential.8. The role of these two groups of cells is discussed.

Journal Article↗

PubMed1992

Effects of genistein, an isoflavone isolated from Genista tridentata, on isolated guinea-pig ileum and guinea-pig ileal myenteric plexus.

The inhibitory action of the major constituent of Genista tridentata L. (Papilionaceae), 4',5,7-trihydroxyisoflavone (genistein), on contractions induced by agonists and electrical field stimulation of smooth muscle was analysed. Genistein inhibited twitches evoked by electrical-stimulation of strips of guinea-pig ileum with an IC50 value of 34 microM. Genistein (34 microM) inhibited contractions of the guinea-pig ileum by several agonists in a non-selective, antispasmodic action and had no effect on inhibition of 3H-ACh release from ileal myenteric plexus. Genistein (34 microM) produces an increase in cAMP levels of guinea-pig ileum which resulted in a smooth muscle relaxation which leads us to think that there must be a blockade of its phosphodiesterase.

Animals↗

PubMed2002

ATP as a putative sensory mediator: activation of intrinsic sensory neurons of the myenteric plexus via P2X receptors.

The mucosal terminals of sensory neurons intrinsic to the wall of the intestine are sensitive to the chemical environment within the lumen. Lumenal stimuli probably release sensory mediators from the mucosal epithelium, which then activate the nerve terminals indirectly. Here, we tested the idea that ATP activates intrinsic sensory nerve terminals in a way consistent with its being a sensory mediator. We made intracellular recordings from intrinsic sensory neurons located in the myenteric plexus [identified as AH neurons, which are neurons with a long-lasting afterhyperpolarization following the action potential (AP)], located within 1 mm of intact mucosa. Focal electrical stimulation of the mucosa was used to locate and map regions innervated by each neuron. Application of ATP (1-2 mm in the pressure pipette) to these regions elicited trains of APs that originated at the sensory terminals. ATP-gamma-S produced a similar response, but alpha,beta-methylene ATP and 2-methylthio-ATP were only weakly active. The P2 receptor antagonist pyridoxalphosphate-6-azophenyl-2',5'-disulphonic acid (PPADS) (60 microm in the bath) abolished the APs evoked by ATP and ATP-gamma-S but spared similar responses evoked by 5-hydroxytryptamine (5-HT). Another P2 receptor antagonist suramin (100 microm in the bath) did not significantly change the number of APs evoked by ATP. Either ATP or alpha,beta-methylene ATP desensitized the ATP-evoked APs; 50% recovery occurred after approximately 5 sec. The number of APs evoked by ATP was reduced, but not abolished, by the selective 5-HT3 receptor antagonist granisetron (1 microm in the bath). ATP was applied to the cell bodies of sensory neurons to investigate whether the cell bodies express the same P2X receptor as the terminals. ATP evoked a fast depolarization associated with a reduction in input resistance and a reversal potential of -11 mV. This depolarization was potentiated by suramin and blocked by PPADS. We conclude that activation of an atypical excitatory P2X receptor by ATP triggers AP generation in the mucosal processes of the sensory neurons; endogenous 5-HT release may also contribute to activation of the nerve terminals. A similar P2X receptor exists on the cell body of the sensory neuron. Together, these data are consistent with a role for ATP as a sensory mediator in gastrointestinal chemosensory transduction.

Action Potentials↗

PubMed2005

Serum from achalasia patients alters neurochemical coding in the myenteric plexus and nitric oxide mediated motor response in normal human fundus.

BACKGROUND AND AIMS: Achalasia is a disease of unknown aetiology. An immune mechanism has been suggested on the basis of previous morphological observations. The objective of this study was to test whether the serum of achalasia patients could reproduce the phenotype and functional changes that occur with disease progression in an ex vivo human model. METHODS: Specimens of normal human fundus were maintained in culture in the presence of serum from patients with achalasia, gastro-oesophageal reflux disease (GORD), or healthy subjects (controls). Immunohistochemical detection of choline acetyltransferase (ChAT), neurone specific enolase (NSE), vasoactive intestinal polypeptide (VIP), nitric oxide synthase (NOS), and substance P was carried out in whole mounts of gastric fundus myenteric plexus. In addition, the effects of achalasia serum on electrical field stimulation (EFS) induced contractions were measured in circular muscle preparations. RESULTS: Serum from achalasia patients did not affect the number of myenteric neurones. Tissues incubated with serum from achalasia patients showed a decrease in the proportion of NOS (-26% of NSE positive neurones; p=0.016) and VIP (-54%; p=0.09) neurones, and a concomitant increase in ChAT neurones (+16%; p<0.001) compared with controls. In contrast, GORD serum did not modify the phenotype of myenteric neurones. Area under the curve of EFS induced relaxations (abolished by N-nitro-L-arginine methyl ester) was significantly decreased following incubation with serum from achalasia patients compared with controls (-7.6 (2.6) v -14.5 (5.0); p=0.036). CONCLUSIONS: Serum from achalasia patients can induce phenotypic and functional changes which reproduce the characteristics of the disease. Further identification of putative seric factors and mechanisms involved could lead to the development of novel diagnostic and/or therapeutic strategies in achalasia.

Adult↗

PubMed1985

Specific antagonism of enteric neural serotonin receptors by dipeptides of 5-hydroxytryptophan: evidence that serotonin is a mediator of slow synaptic excitation in the myenteric plexus.

Research on the role of serotonin (5-hydroxytryptamine, 5-HT) in the function of the enteric nervous system has been impeded by the lack of specific inhibitors of the enteric neural actions of 5-HT. Saturable, reversible, high affinity enteric binding sites for 3H-5-HT have recently been characterized and radioautographically located. Affinity for the 3H-5-HT binding site requires an indole ring substituted with a free hydroxyl group. These 3H-5-HT binding sites have been proposed to be enteric neural 5-HT receptors. This hypothesis was tested in the current study by comparing the ability of compounds to inhibit the binding of 3H-5-HT with their electrophysiologically determined actions on myenteric neurons. 5-Methoxytryptamine did not inhibit the binding of 3H-5-HT to enteric membranes and neither mimicked nor antagonized the effects of 5-HT on the membrane potential of myenteric neurons. Two dipeptides of 5-hydroxytryptophan, N-acetyl- and N-hexanoyl-5-hydroxytryptophyl-5-hydroxytryptophan amide (5-HTP-DP and N-hex-5-HTP-DP) inhibited the binding of 3H-5-HT (K1 = 0.25 microM for 5-HTP-DP and 1.19 microM for N-hex-5-HTP-DP). 5-HTP-DP applied by pressure microejection or superfusion (10 microM) antagonized the slow postsynaptic depolarization of myenteric neurons evoked by microejection of 5-HT. 5-HTP-DP also blocked the 5-HT-induced presynaptic reduction in amplitude of nicotinic fast synaptic potentials; however, 5-HTP-DP itself did not affect these responses. Moreover, 5-HTP-DP also failed to affect responses of myenteric neurons to microejected substance P, their muscarinic response to acetylcholine, or antidromic action potentials. In contrast, both dipeptides blocked the slow synaptic potentials seen in type II/AH neurons following stimulation of fiber tracts in interganglionic connectives. These data support the hypotheses that enteric 3H-5-HT binding sites are enteric neural 5-HT receptors, that dipeptides of 5-hydroxytryptophan are specific antagonists at these receptors, and that 5-HT is one of the mediators of slow synaptic potentials in the myenteric plexus.

5-Hydroxytryptophan↗

PubMed2000

IgG-mediated cytotoxicity to myenteric plexus cultures in patients with paraneoplastic neurological syndromes.

Autoantibodies against neuronal and tumour proteins have been described in many paraneoplastic neurological syndromes (PNS), but it is not clear whether these antibodies are pathogenic or simply a useful diagnostic tool. We took seven sera that were positive on routine screening for antineuronal antibodies and the IgG fractions. As controls we used sera from health blood-donors, other neurological autoimmune diseases and patients with SCLC without PNS. We tested them on dissociated rat myenteric plexus cultures for cytotoxic effects. After incubation for 24 h, cytotoxicity was determined by a double fluorescence test (calcein green for living cells and ethidium homodimer-1 for dead cells). We found an increased cell death rate in cultures incubated with the PNS sera, compared with all controls (P< 0.05). Isolated IgG fractions were also cytotoxic whereas the IgG-free serum fraction did not show any significant increase in cytotoxicity. After incubation with PNS IgG, FACS analysis revealed an increased cytotoxicity rate only of the neurones, but not the glial cells. Our results indicate that in PNS a complement-independent, antibody-mediated cytotoxicity against neurones may contribute to the pathogenesis of these syndromes.

Animals↗

PubMed1995

Isolation of enteric ganglia from the myenteric plexus of adult rats.

Enteric neurons and glia cells were isolated from adult Sprague Dawley rats. A procedure is described using a combination of microdissection and mechanical dissociation after enzyme treatment which yields large numbers of cell clusters suitable for tissue culture and grafting into the injured spinal cord. Differentiated enteric ganglia remained viable for at least 5 days in vitro. Cultured neurons expressed histochemical reactivity for acetylcholinesterase and nicotinamide adenine dinucleotide phosphate diaphorase. Nestin positive glia, which represented a population of non-myelinating enteric Schwann cells, could also be identified in cultures maintained 5 days or longer in vitro. The myenteric plexus of adult rats can provide a readily available source of neurons and Schwann cells for grafting to the central nervous system.

Animals↗