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PubMed2000

Inflammation-induced impairment of enteric nerve function in nematode-infected mice is macrophage dependent.

Trichinella spiralis infection in rodents is associated with suppression of ACh release from myenteric plexus that can be mimicked by macrophage-derived cytokines. We verified the presence of a macrophage infiltrate in the intestine during T. spiralis infection and determined the extent to which this cell type is responsible for the neural changes. C57BL/6 mice were infected with 375 T. spiralis larvae by gavage, and the presence of macrophages (F4/80 positive) in the jejunum was determined immunohistochemically. In another experiment, infected mice were treated intravenously with liposomes containing dichloromethylene diphosphonate (clodronate, Cl(2)MDP), which causes apoptosis of macrophages, and killed at postinfection day 6, and jejunal tissues were evaluated for the presence of F4/80-positive cells and for [(3)H]ACh release from the myenteric plexus. Infection caused an infiltration of F4/80-positive cells into the intestinal mucosa, muscle layers, and myenteric plexus region and a significant suppression of ACh release (50%). Depletion of F4/80-positive macrophages using Cl(2)MDP-containing liposomes prevented the suppression in [(3)H]ACh release, identifying macrophages as the cell type involved in the functional impairment of enteric cholinergic nerves.

Acetylcholine↗

PubMed2006

The pathogenesis of idiopathic megacolon.

BACKGROUND: Even today, the pathogenesis of idiopathic megacolon is still a subject of controversy. Anomalies of the gastrointestinal autonomous nervous system or of the smooth muscle of the muscularis propria are being considered. METHODS: Sixty-three idiopathic megacolon resections between 1997 and June 2004 were investigated. The native specimens were coiled caudo-cranially and cryostat-cut. Connective tissue was stained with picric acid/Sirius red after Delauney fixation. Immunohistochemistry was performed for collagen types I, II, III and IV, as well as smooth muscle actin, vimentin, desmin fibronectin and CD117 for interstitial cells of Cajal. The enteric nervous system was examined by enzyme histochemistry for acetylcholine-esterase, lactate dehydrogenase, succinic dehydrogenase and nitroxide synthase. RESULTS: Histologically, idiopathic megacolon was characterized by a total atrophy of the collagenous tendinous connective tissue membrane of the myenteric plexus and the tendinous collagen fibre net of the muscularis propria. Immunohistochemically, mainly collagen type III was missing in the muscularis propria. Interestingly, the incidence of idiopathic megacolon in those of the female sex was seven times more frequent than in the male sex. The myenteric plexus was normal in the majority of patients. Interstitial cells of Cajal, collagen II and IV, as well as smooth muscle actin, desmin and fibronectin showed no consistent alteration. CONCLUSION: A normally structured tendinous fibre net of muscularis propria is an essential prerequisite for effective gut peristalsis. Atrophy of the tendinous fibre net abolishes peristalsis and allows for unlimited distension of the colon. A diagnosis of idiopathic megacolon can reliably be made on a collagen stain. The normal findings of myenteric plexus support the hypothesis that a primary metabolic defect of muscularis propria may be the underlying cause of idiopathic megacolon.

Adolescent↗

PubMed1992

Differential inhibition of cholinergic and noncholinergic neurogenic contractions by 5-hydroxytryptamine1A receptor agonists in guinea pig ileum.

Previous studies have shown that 5-hydroxytryptamine1A (5-HT1A) receptors are localized only to a subset of myenteric neurons in guinea pig ileum; the purpose of this study was to determine the possible functional significance of this differential receptor localization. Nerve-mediated contractions of the longitudinal muscle, myenteric plexus of guinea pig ileum were studied in vitro. Contractions were evoked by single transmural electrical stimuli (0.5-msec duration, at 0.1 Hz; cholinergic) or trains of stimuli (10 or 20 Hz for 1 sec; noncholinergic; scopolamine, 1 microM present). The 5-HT1A agonist, 8-hydroxy-2-(n-dipropylamino)tetralin (DPAT), reduced cholinergic contractions by no more than 14% in the concentration range of 0.001 to 0.3 microM. At high concentrations (1 to 100 microM), DPAT inhibited longitudinal muscle, myenteric plexus contractions; the EC50 was 6 microM. 5-Hydroxytryptamine (5-HT) and 5-carboxamidotryptamine (5-CT) reduced longitudinal muscle, myenteric plexus contractions by a maximum of 35% and 24% at 100 and 30 microM, respectively. Spiperone and 1-(2-methoxyphenyl)-4-[4-(2-phthalimidobutyl]piperazine (NAN-190), two 5-HT1A receptor antagonists, did not block DPAT-induced inhibition of cholinergic contractions. DPAT (3, 10 and 30 microM) shifted histamine concentration-response curves to the right in an apparently competitive manner; Schild analysis yielded a pA2 of 5.2. DPAT (3, 10, 30 and 100 microM) also shifted bethanechol concentration-response curves to the right in an apparently competitive manner; Schild analysis yielded a pA2 of 5.5. These data indicate that DPAT blocks histamine and muscarinic receptors on longitudinal muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1985

The enteric neural receptor for 5-hydroxytryptamine.

An enteric neural receptor for serotonin (5-HT) has been characterized. This receptor was assayed, using 3H-5-HT as a radioligand, by rapid filtration of isolated enteric membranes and by radioautography. In addition, intracellular recordings were made from ganglion cells of the myenteric plexus. High affinity, saturable, reversible, and specific binding of 3H-5-HT was demonstrated both to membranes of the dissected longitudinal muscle with adherent myenteric plexus and the mucosa-submucosa. Radioautographs showed these 3H-5-HT binding sites to be in myenteric ganglia and in a broad unresolved band at the mucosal-submucosal interface. Antagonists active at receptors for other neurotransmitters than 5-HT, at either of the two known types of CNS 5-HT receptor, and at 5-HT uptake sites on serotonergic neurons failed to inhibit binding of 3H-5-HT. The structural requirements of analogues for binding to the enteric 5-HT receptor matched the known pharmacology of M or neural 5-HT receptors. A novel 5-HT antagonist was found. This compound, N-acetyl-5-hydroxytryptophyl-5-hydroxytryptophan amide (5-HTP-DP), antagonized the action of 5-HT on type II/AH cells of the myenteric plexus but did not affect the release or actions of acetylcholine (nicotinic or muscarinic) or substance P. 5-HTP-DP was also an equally potent displacer of 3H-5-HT from its binding sites on enteric membranes. It is concluded that the sites responsible for specific binding of 3H-5-HT are enteric M or neural 5-HT receptors. These receptors differ from those now known to be present in the CNS.

5-Hydroxytryptophan↗

PubMed1999

GABA(A) receptor subunit messenger RNA expression in the enteric nervous system of the rat: implications for functional diversity of enteric GABA(A) receptors.

GABAergic neurons occur in the myenteric plexus and submucosa and their innervations of the gut, where GABA stimulates motor neurons, and non-neural cells via "central type" GABA(A) receptors. These receptors occur on half of the neurons in the rat intestine. The GABA(A) receptor is a ligand-gated chloride channel constructed from different subunit families (alpha, beta, gamma, delta, epsilon). In rat these exist as subtypes, alpha1-6, beta1-3, gamma1-3 and delta, defining the clinically relevant pharmacological features of GABA(A) receptors. However, the identity, distribution, and abundance of enteric GABA(A) receptor subunits are unknown. To identify and map the regional expression of GABA(A) receptor subunit messenger RNAs in the enteric nervous system, we assayed enteric RNA from the ileum of Sprague-Dawley rats by reverse transcription-polymerase chain reaction for alpha1-6, beta 1-3, gamma1-3, and delta subunit messenger RNAs. Subunit messenger RNA localization, was probed by in situ hybridization. Reverse transcription-polymerase chain reaction analysis of RNA from myenteric and submucosal nerve layers revealed the expression alpha1, alpha3, beta2, beta3, gamma1 and gamma3 subunit messenger RNAs. Little alpha4 and alpha6 and no alpha2, beta1, gamma2 or delta subunit messenger RNA were detected. In situ hybridization revealed that transcripts for alpha1, alpha3, alpha5 and beta2 subunits occur in both myenteric and submucous ganglia. However, beta3 messenger RNA was found only in myenteric plexus. The gamma1 subunit messenger RNA was also restricted to the cells in the myenteric plexus while gamma3 was found in cells of both nerve layers. In this study of the subunit messenger RNA expression profile of GABA(A) receptors within the enteric nerve layers we show an abundant, diverse and widespread distribution that is unique in comparison to the CNS. The distinctive and heterogeneous distribution of enteric GABA(A) subunits may be important in the integration of neural control of gut function.

Animals↗

PubMed1993

Neuroplasticity in the smooth muscle of the myenterically and extrinsically denervated rat jejunum.

The objective of this study was to examine the effects of two different denervation procedures on the distribution of nerve fibers and neurotransmitter levels in the rat jejunum. Extrinsic nerves were eliminated by crushing the mesenteric pedicle to a segment of jejunum. The myenteric plexus and extrinsic nerves were eliminated by serosal application of the cationic surfactant benzyldimethyltetradecylammonium chloride (BAC). The effects of these two denervation procedures were evaluated at 15 and 45 days. The level of norepinephrine in whole segments of jejunum was initially reduced by more than 76% after both denervation procedures, but by 45 days the level of norepinephrine was the same as in control tissue. Tyrosine hydroxylase (noradrenergic nerve marker) immunostaining was absent at 15 days, but returned by 45 days. However, the pattern of noradrenergic innervating axons was altered in the segment deprived of myenteric neurons. Immunohistochemical studies showed protein gene product 9.5 (PGP 9.5)-immunoreactive fibers in whole-mount preparations of the circular smooth muscle in the absence of the myenteric plexus and extrinsic nerves. At 45 days, the number of nerve fibers in the circular smooth muscle increased. Vasoactive intestinal polypeptide (VIP)-immunoreactive fibers, a subset of the PGP 9.5 nerve fibers, were present in the circular smooth muscle at both time points examined. Choline acetyltransferase (CAT) activity and VIP and leucine enkephalin levels were measured in separated smooth muscle and submucosa-mucosal layers of the denervated jejunum. VIP and leucine-enkephalin levels were no different from control in tissue that was extrinsically denervated alone. However, the levels of these peptides were elevated two-fold in the smooth muscle 15 and 45 days after myenteric and extrinsic denervation. In the submucosa-mucosa, VIP and leucine enkephalin levels also were elevated two-fold at 15 days, but comparable to control at 45 days. CAT activity was equal to control in the smooth muscle but elevated two-fold in the submucosa-mucosa at both times. These results provide evidence for innervation of the circular smooth muscle by the submucosal plexus. Moreover, these nerve fibers originating from the submucosal plexus proliferate in the absence of the myenteric plexus. Furthermore, the myenteric neurons appear to be essential for normal innervation of the smooth muscle by the sympathetic nerve fibers. It is speculated that the sprouting of the submucosal plexus induced by myenteric plexus ablation is mediated by increased production of trophic factors in the hyperplastic smooth muscle.

Animals↗

PubMed1999

Opioid peptide mRNA expression in the colon of the rat.

Since the discovery of opioid peptides, several immunohistochemical and radioimmunological studies have demonstrated their localization in the gastrointestinal tract without demonstrating the localization of their common precursor. The present study describes the distribution and the colocalization of proenkephalin and prodynorphin messenger RNAs (mRNAs) in the colon of rat by in situ hybridization. Proenkephalin and prodynorphin mRNAs were found in myenteric plexus, but not in the submucous plexus or in the mucosa. In myenteric plexus, the number of neurons expressing proenkephalin is 2.5 times greater than that of the neurons expressing only prodynorphin. Furthermore, double in situ hybridization histochemistry indicates that at least three groups of opioid neurons can be distinguished, those containing proenkephalin and prodynorphin mRNAs together, and those containing only proenkephalin mRNA or only prodynorphin mRNA.

Animals↗

PubMed2006

Contributions to the micro-anatomical evaluation of the ratio between the muscular tunic structures of the oesophagus. Biomechanical, anatomic and clinical implications.

The aim of our research is to make a microanatomical evaluation of the ratios of the structural elements of the oesophagus muscular tunic and suggest a new perspective in the general knowledge about this tubular organ. The visualisation of the structural elements was done using classical microanatomical methods Hematoxylin-Eosin for general orientation, Van Gieson for picrofuxinophile collagen fibers and Gömöri for reticuline fibers. The neurofilaments were identified using silver impregnation on Cajal block. The examination of the sections was made with the Nikon Eclipse 600 photomicroscope. The images were taken and processed using a computer with LuciaNet licensed Microsoft. The co-existence in the architecture of the oesophagus of two microcinematic systems structurally divergent, but functionally convergent represents microanatomical arguments for the nomination of a new type of muscles--the oesophageal muscle--anatomo-functionally different from the skeletal striate muscle, from the smooth visceral muscle, from the cardiac muscle or from the embryonic type muscle of the excitoconductor system. The extra cellular matrix of the muscular tunic of the oesophagus contributes to the organization of the endo- and peri-misium, as well as to the three structures involved in the biomechanics of the oesophageal muscle: the connective-vascular septa, the microtendons that have in their structure receptors of the peristaltic reflex and, finally, the lamina propria myenterica strewed with numerous neuronal structures. The co-existence of the stereo-distribution of the monostructured fascicles (skeletal muscular fibers or smooth muscular cells) with bistructured fascicles (skeletal-smooth) gives the oesophagus a heterogeneous architecture. Lamina propria myenterica, which realizes the border between the circular and longitudinal strata, contains two neuronal structures of its own, but anatomically inserted the neural myenteric plexus which is equivalent to the Auerbach plexus and the neuroganglion of the myenteric plexus, equivalent to the visceral neuroganglion Cajal-Retzius.

Adult↗

PubMed1985

Physiological responses of guinea-pig myenteric neurons secondary to the release of endogenous serotonin by tryptamine.

Intracellular recordings showed that administration of pulses of tryptamine mimicked one of the actions of serotonin (a slow depolarization associated with an increased input resistance) on type II/AH neurons of the myenteric plexus. After superfusion at high concentration tryptamine initially acted like serotonin, but then blocked the action of serotonin on these cells. Measurements of the release of preloaded [3H]serotonin or [3H]norepinephrine revealed that tryptamine is a potent releaser of these labeled amines; this release is Ca2+ independent but temperature dependent. Moreover, incubation with tryptamine depleted the myenteric plexus of endogenous serotonin. Since tryptamine has previously been demonstrated not to inhibit the binding of [3H]serotonin to its enteric neural receptor we framed the hypothesis that the serotonin-releasing action of tryptamine is responsible for its ability to mimic serotonin when given in pulses or to desensitize serotonin receptors through the prolonged release of serotonin when it is superfused. This hypothesis was tested by examining the action of tryptamine on the serotonin-mediated slow excitatory postsynaptic potentials evoked in type II/AH neurons by fiber tract stimulation. Tryptamine superfusion antagonized these slow potentials as predicted. Moreover, after a long time when endogenous serotonin was depleted, the response of type II/AH neurons to exogenous serotonin recovered but the slow synaptic potential did not. The action of tryptamine on this neuron was relatively specific. When the slow synaptic potential and serotonin responses were blocked by tryptamine the type II/AH neurons still responded to acetylcholine. Fast excitatory postsynaptic potentials were not affected by tryptamine. Furthermore, other types of neurons (I/S) and other neuronal responses to serotonin (such as a fast depolarization with decreased input resistance or presynaptic inhibition of acetylcholine release) were not blocked by tryptamine. Finally, radioautographic studies revealed a neural uptake of tryptamine in the chemically sympathectomized myenteric plexus; however, the distribution of tryptamine in the plexus was different from that of serotonin and was not blocked by excess non-radioactive serotonin. Therefore tryptamine does not enter myenteric neurons via the specific serotonin uptake mechanism; however, zimelidine, found to be a selective inhibitor of the enteric uptake of serotonin, antagonized the release of serotonin by tryptamine and attenuated the effect of tryptamine on responses to serotonin.(ABSTRACT TRUNCATED AT 400 WORDS)

5-Methoxytryptamine↗

PubMed2002

Distribution and effects of PACAP, VIP, nitric oxide and GABA in the gut of the African clawed frog Xenopus laevis.

The distribution and possible effects on gastrointestinal motility of pituitary adenylate cyclase-activating polypeptide (PACAP), vasoactive intestinal polypeptide (VIP), nitric oxide and gamma-amino-butyric acid (GABA) were investigated in the African clawed frog (Xenopus laevis) using immunohistochemistry and in vitro strip preparations. PACAP- and VIP-immunoreactive nerve fibres were common in the myenteric plexus as well as in the longitudinal and circular muscle layers all along the gastrointestinal tract. Double labelling demonstrated a close correlation between PACAP and VIP immunoreactivities, indicating that the two neurotransmitters are colocalised within the enteric nervous system. Occasionally, PACAP- and VIP-positive nerve cell bodies were seen in the myenteric or submucous plexa. In addition, VIP immunoreactivity coexisted with helospectin immunoreactivity. Nitric oxide synthase (NOS)-immunoreactive nerve cells were found in the myenteric plexus at an average density for the whole gastrointestinal tract of 4584 +/- 540 cells cm(-2). The NOS-immunoreactive nerve cells were usually multipolar with an average size of 11.3 +/- 3.7 x 23.2 +/- 6.6 microm. Some NOS-immunoreactive nerve fibres were VIP-immunoreactive but not all VIP-positive fibres showed NOS immunoreactivity. GABA immunoreactivity was found in nerve fibres and nerve cells in the myenteric plexus of all regions of the gut. Few GABA-immunoreactive nerve fibres were VIP-immunoreactive. PACAP 27, VIP, sodium nitroprusside (a nitric oxide donor; NaNP) and GABA caused similar responses on spontaneously contracting circular preparations of the cardiac stomach of X. laevis. The mean force developed was decreased, mainly by a reduction in resting tension, while the amplitude of contractions was not necessarily affected. The NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) increased the mean force developed, indicating a nitrergic tone in the preparations. In contrast, PACAP 27, VIP, NaNP, GABA and L-NAME had no significant effect on longitudinal strip preparations from the duodenum. These results indicate that PACAP, VIP, nitric oxide and GABA, which are known to be important inhibitory neurotransmitters in other vertebrates, are widely spread in the enteric nervous system of Xenopus laevis and may be involved in the inhibitory control of gastric motility. Although no effect of PACAP, VIP, nitric oxide or GABA on the longitudinal strips of the duodenum was seen in this study, this does not rule out the possibility that they might play an important role in controlling intestinal motility as well.

Animals↗

PubMed1977

Discrimination between nicotinic receptors in vertebrate ganglia and skeletal muscle by alpha-bungarotoxin and cobra venoms.

1. We have used snake neurotoxins, alpha-bungarotoxin and venoms from Naja naja siamensis and Naja nivea, to distinguish the nicotinic receptors of ganglia from those of skeletal neuromuscular junctions. 2. These neurotoxins failed to block responses of isolated guinea-pig longitudinal muscle with adherent myenteric plexus to the nicotinic agonists, nicotine or dimethylphenylpiperazinium, to acetylcholine (ACh), or to electrical field stimulation. 3. The toxins failed to affect responses of the isolated guinea-pig stomach to pregnaglionic stimulation by way of the vagus nerves or of the vas deferens to preganglionic stimulation via the hypogastric nerves. 4. Snake neurotoxins did not block non-adrenergic inhibitory responses of the rabbit small intestine to nicotine or electrical field stimulation. 5. Neurotoxins were ineffective blockers against nicotinic agonists in new-born rabbit or embryonic chick intestine. 6. Attempts to increase the penetration of the toxins into tissues with dimethylsulphoxide, exposure to hypertonic solutions, or to ethylene-diaminetetracetic acid did not enable the toxins to act as nicotinic antagonists. 7. In contrast to diaphragmatic or oesophageal skeletal neuromuscular junctions no binding of rhodamine or tritium labelled toxins to structures in ganglia could be detected. 8. No potential permeability barriers were found by electron microscopy of the ganglia of the guinea-pig myenteric plexus. 9. The tracers, lanthanum ion and ruthenium red, readily penetrated into all regions of the myenteric plexus including synaptic gaps. 10. It is concluded that the failure of snake neurotoxins to act as nicotinic antagonists or to bind to ganglia is not due to their inability to reach ganglionic nicotinic receptors. Therefore, it is likely that ganglionic nicotinic receptors are different from those of the skeletal neuromuscular junction.

Action Potentials↗

PubMed1988

An electrophysiological study of the projections of motor neurones that mediate non-cholinergic excitation in the circular muscle of the guinea-pig small intestine.

The projections of neurones that produce the fast non-cholinergic excitatory junction potentials (e.j.p.s) in the circular muscle were analysed in the isolated ileum of the guinea-pig. Standard intracellular microelectrode techniques were used to record the amplitudes of such e.j.p.s in response to short trains of stimuli from transmural electrodes. Projections of the neurones around the circumference of the intestine were determined by plotting the change in e.j.p. amplitude with distance from longitudinally placed electrodes. Projections in the oral and anal directions were examined by recording at varying distances from transversely placed electrodes, and also by recording responses elicited close to longitudinal electrodes at various distances from lesions made 3-5 days earlier to interrupt orally and anally directed pathways. Experiments were performed in the presence of hexamethonium to determine the projections of the final motor neurones and in the absence of the drug to examine the projections of excitatory inputs to these neurones. With hexamethonium present, there was a decline in e.j.p. amplitude to 7.5% of maximum at 12 mm (a half circumference) from longitudinal stimulating electrodes. The decline was much less if hexamethonium was not present, and slightly greater if the myenteric plexus was removed. Thus, excitatory motor neurones and cholinergic neurones that impinge upon them both project circumferentially. When the longitudinal muscle and myenteric plexus were removed, and 3-5 days allowed for terminals to degenerate, no e.j.p.s could be recorded in the circular muscle, indicating that the fibres reach the circular muscle from the myenteric plexus. Following transverse lesions, substantial deficits in excitatory transmission only occurred within 1 mm oral or anal to the lesions indicating that the majority of neurones have only short projections along the intestine. A slight deficit in e.j.p. amplitude, up to 20%, was observed extending to about 5 mm oral; but normal transmission was restored by about 10 mm for the lesions. Thus there is a minority of excitatory motor neurones with oral projections up to about 10 mm in length. Results with transmural stimulation showed that these nerve fibres can cause excitation both when orthodromically and when antidromically stimulated, indicating that they provide collaterals along their lengths. With no hexamethonium present, e.j.p.s exhibited little decrement in amplitude over distances of over 30 mm oral or anal indicating that there are both ascending and descending cholinergic pathways that impinge on the final motor neurones.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed2001

Three-dimensional morphology of gut innervation in total intestinal aganglionosis using whole-mount preparation.

BACKGROUND: Total intestinal aganglionosis (TIA) is a rare form of Hirschsprung's disease (HD). The aim of this study was to examine the 3-dimensional morphology of the myentric plexus of the entire gastrointestinal tract in a newborn with total intestinal aganglionosis. METHODS: Whole-mount preparations were made of the entire gastrointestinal tract using NADPH-diaphorase histochemistry and c-kit (a marker of interstitial cells of Cajal) immunohistochemistry. RESULTS: Whole-mount preparations of the esophagus, stomach, and duodenum showed 3-dimensional morphology of the myenteric plexus forming a meshlike network of nerve fibers, connected to each other and to ganglia. There were large numbers of NADPH-diaphrase-positive nerve fibers between the muscle fibers in the circular muscle layer. In esophagus, stomach, and duodenum, c-kit-positive interstitial cells of Cajal (ICC) formed a 3-dimensional network between the two muscle layers and also were abundant within the circular muscle layer. In the jejunum, ileum, and colon, the myenteric plexus was absent and was replaced by hypertrophic nerve bundles that stained weakly with NADPH-diaphrase. Circular muscle layer completely lacked NADPH-diaphrase-positive nerve fibers. The c-kit-positive ICCs in the jejunum, ileum, and colon were sparse and localized mainly around the nerve trunks between the circular and longitudinal muscle layers. CONCLUSIONS: Whole-mount preparation is an elegant 3-dimensional technique in which the relationship of branching and interconnecting nerve fibers to each other and to muscle can be seen clearly. Absence of myenteric plexus, lack of nitrergic innervation, and depletion of interstitial cells of Cajal in the bowel wall throughout the small and large bowel contribute to the inability of the smooth muscle to relax, thereby causing lack of peristalsis in TIA.

Colon↗

PubMed2005

Examination of the role of cholinergic myenteric neurons with the impairment of neural reflexes in the ileum of c-kit mutant mice.

Our previous study showed that impairment of ascending and descending neural reflexes in the ileum of the c-kit mutant, W/W(V), mice is due to a loss of interstitial cells of Cajal present at the myenteric plexus region (ICC-MY) in the mutant. In the present study, cholinergic interneurons were thought to be involved in these pathways, since hexamethonium, an antagonist of the nicotinic ACh receptor, significantly inhibited both neural reflexes in wild type mice. Therefore, we examined whether the loss of ICC-MY affects cholinergic interneurons involved in these pathways. Immunohistochemistry with anti-choline acetyltransferase revealed that there was no difference in the numbers of immunopositive cells in the myenteric plexus region between the wild type and mutant mice. In addition, there was no difference in the extent of spontaneous and EFS-evoked ACh release from longitudinal muscle with myenteric plexus preparations between the wild type and mutant mice. Exogenously added nicotine induced contraction or relaxation of ileal circular muscle in the absence or presence of atropine, respectively, to a similar extent in both the wild type and mutant mice. These results suggest that loss of ICC-MY resulted in an impairment of the ascending and descending reflex pathways at the step before activation of cholinergic interneurons.

Animals↗

PubMed1989

Opioids can enhance and inhibit the electrically evoked release of methionine-enkephalin.

The stimulated (40 Hz) release of enkephalin from the myenteric plexus can be modulated by multiple types of opiate receptor. The direction of the modulation is not fixed but is bimodal. Both an inhibition and an enhancement of evoked release is observed depending on the concentration of opioid agonist that is used. Each of these effects can be antagonized by naloxone. Following pretreatment of guinea pig myenteric plexus in vitro with forskolin (0.5 microM) or the lipid soluble cAMP analog 8-(4-chlorphenylthio)-cAMP (8-CPT-cAMP; 100 microM) the inhibition of stimulated Met-enkephalin release that is produced by sufentanil (10(-8) M), [D-Pen2-D-Pen5]enkephalin (DPDPE, 10(-8) M) or dynorphin (10(-7) M) is no longer observed. On the contrary, in forskolin- or 8-CPT-cAMP treated myenteric plexus a previously inhibitory concentration of the above opioids now produces an enhancement of the magnitude of the stimulated Met-enkephalin release. Excitatory responses (enhanced release) to lower concentrations of sufentanil (1 nM) or DPDPE (5 nM) are not affected by pretreatment with the same concentration of forskolin or 8-CPT-cAMP. These data suggest that the ability of opioids to enhance or inhibit evoked enkephalin release is mediated via different biochemical processes (separate second messenger systems). This could imply that the opioid enhancement of enkephalin release is due to a direct facilitation of release and not to disinhibition. The ability of opioids to enhance the release of at least some neurotransmitters should be taken into account when attempting to explain the physiological sequelae of the acute and chronic effects of narcotics.

Action Potentials↗

PubMed1998

Changes in muscularis externa of rat small intestine after myenteric ablation with benzalkonium chloride: electron microscopic and morphometric study.

The influence of the intrinsic innervation on the muscularis externa of the rat small intestine was studied by chemical ablation of the myenteric plexus with benzalkonium chloride (BAC). The resulting severe hypertrophy (cell hypertrophy of 96-133% and hyperplasia) differs from working hypertrophy by the distribution and degree of muscle thickening and by characteristics of the extracellular matrix: narrowing of muscle interspaces of 43%; lack of increased collagen; changes in the ratio of interstitial cells of Cajal (ICCs) to fibroblasts from 1.6:1 to 0.8:1 with no numerical decrease in either type of cell; decreased interconnections of ICCs to muscles and nerves due to deformed ICCs; a 197% increase in vascularization (capillaries, venules) and lymphatics in both muscle layers and in the myenteric plexus cleft, possibly initiated by release of fibroblast growth factor from myelin fragmentation after nerve damage; and increased macrophages, plasma cells, monocytes and mast cells in the myenteric plexus cleft. These all signify the neural influence on the morphodifferentiation of the muscularis externa in concert with the extracellular matrix components.

Animals↗

PubMed1996

Distribution of peptide-containing nerve fibres in achalasia of the oesophagus.

In this study the innervation of the normal human oesophagus was compared with samples taken from 12 patients undergoing Heller's cardiomyotomy for achalasia. The distribution of all nerve fibres in the oesophageal wall was revealed by immunoreactivity to neuron specific enolase and subpopulations of nerve fibres were revealed by immunoreactivity to vasoactive intestinal peptide, neuropeptide Y, enkephalin and substance P. In healthy oesophagus, many nerve fibres immunoreactive for vasoactive intestinal peptide and neuropeptide Y were present in the circular and longitudinal muscle layers of the oesophageal wall and in the cardia of the stomach, whereas fibres immunoreactive for enkephalin and substance P were uncommon. Neuropeptide Y-reactive fibres were commonly seen around blood vessels. In the myenteric plexus cell bodies reactive for vasoactive intestinal peptide and neuropeptide Y were prevalent, as were varicose and non-varicose fibres. In contrast, samples from patients with achalasia revealed few nerve fibres immunoreactive for vasoactive intestinal peptide or neuropeptide Y in either circular or longitudinal muscle, suggesting damage to the inhibitory motor neurons to the muscle layers. Very few fibres were found that were reactive for neuron-specific enolase, indicating that other fibre population (e.g. excitatory cholinergic motor neurons) are also damaged in achalasia. These abnormalities were observed in biopsies from both the constricted and dilated portions of the oesophagus, but the pattern of innervation in the gastric cardia was normal. Myenteric ganglion cells were seen in the oesophagus in only two patients and varicose nerve fibres in the myenteric plexus were uncommon. Neuropeptide Y-reactive perivascular nerve fibres were still found in achalasia as well as non-varicose nerve fibres in the myenteric plexus. These findings indicate damage to all intrinsic neurons in the oesophageal wall in achalasia; however, extrinsic nerve fibres appear to be intact.

Adult↗

PubMed2004

Multiple myenteric networks in the human appendix.

The general histological organization of the appendix, including its innervation, is believed to be generally similar to that of the large intestine. However, several authors described an unusual arrangement of the myenteric ganglia within the appendiceal muscle, but conflicting reports do not allow clear conclusions on this matter. The aim of this work was to examine the appendiceal innervation in detail. The myenteric plexus of the human appendix was examined using sections and whole mount preparations. Human small and large intestines were used for comparison. The nerves were stained using immunohistochemistry, enzyme histochemistry for NADPH-diaphorase, and vital staining with 4-(4-diethylaminostyryl)-methylpyridinium iodide. Appendices from rabbits were also studied. In most cases, the innervation of the external muscle of the appendix consisted of three concentric networks of ganglia. These networks were located both between the circular and longitudinal muscle layers and within them. The middle network made connections with the other two. Such arrangement was not observed in the human small and large intestines. The myenteric plexus in the rabbit appendix displayed a much smaller degree of three-dimensional distribution compared with that of the human appendix. It is concluded that the myenteric plexus in the human appendix consists of several distinct networks, and appears to be unique in comparison with the other parts of the intestine.

Adolescent↗