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PubMed1985

Neuropeptides in the gastrointestinal canal of Necturus maculosus. Distribution and effects on motility.

The presence and distribution of regulatory peptides in nerves and endocrine cells of the stomach, intestine and rectum of a urodele amphibian, the mudpuppy, Necturus maculosus, was studied immunohistochemically in sections or whole-mount preparations of the gut wall. The effect of the occurring peptides on gut motility was studied in isolated strip preparations of circular and longitudinal smooth muscle from different parts of the gut. Bombesin-, neurotensin-, substance P- and VIP-like immunoreactivity was present in abundant nerve fibres in the myenteric plexus of both stomach, intestine and rectum. Single fibres or bundles were present in the circular muscle layer and in a well-developed deep muscular plexus in the intestine and rectum. Immunoreactive nerve cells were found in the myenteric plexus of the stomach, intestine (neurotensin only) and rectum. Gastrin/CCK-like immunoreactivity was observed only in a few fibres in stomach and rectum. Endocrine cells containing bombesin-, met-enkephalin-, gastrin/CCK-, neurotensin-, somatostatin- or substance P- like immunoreactivity were present in the mucosa. The effect of bombesin was an inhibition of the rhythmic activity in circular muscle preparations and in longitudinal muscle from the rectum, while longitudinal muscle from the stomach usually responded with a weak increase in tonus. Neurotensin, like-bombesin, was inhibitory on the spontaneous rhythmic activity of circular muscle throughout the gut, while the effect on longitudinal muscle was an increase in tonus. Met-enkephalin and substance P increased the tonus of all types of preparations, and often, in addition, initiated a rhythmic activity superimposed on this maintained tonus. VIP had a general inhibitory effect on the preparations, decreasing tonus and/or abolishing rhythmic activity. It is concluded that bombesin-, neurotensin-, substance P- and VIP-like peptides are present in nerves throughout the urodele gut and may have physiological functions in regulating the motility of the gut. The gastrin/CCK-like peptide present in nerves of the stomach and rectum may affect the function of these parts of the gut. The regulatory peptides present in endocrine cells may, perhaps with the exception of the somatostatin-like peptide, affect the motility humorally.

Animals↗

PubMed1985

Pelvic motility and response to intraluminal bisacodyl in slow-transit constipation.

The resting motility of the pelvic colon was studied in 28 patients with constipation and compared with control subjects and patients with diarrhea. Colonic activity in patients who had been shown to have slow colonic transit was not significantly different from controls. In contrast, activity in patients who complained of constipation but who were found to have normal colonic transit time was increased (P less than 0.02). The response of the pelvic colon to the introduction of a surface-acting laxative was studied in 18 patients with slow-transit constipation. Eleven patients developed progressive peristaltic waves, while in 7 there was no response. It is possible that the relative inactivity of the colon in the latter group is due to a disorder of the myenteric plexus. If so, the bisacodyl stimulation test may distinguish patients with an abnormal myenteric plexus from those in whom it is normal.

Adult↗

PubMed2004

Apoptosis and autoimmunity as proposed pathogenetic links between Helicobacter pylori infection and idiopathic achalasia.

Achalasia is a disorder of the oesophagus characterised by increased lower oesophageal sphincter (LOS) tone, lack of LOS relaxation with swallowing and aperistalsis of the body of the oesophagus. The aetiology and pathogenesis of idiopathic achalasia are still unclear, although a viral cause, genetic influences (associations with HLA loci) and autoimmune processes have been postulated. Degeneration and significant loss of nerve fibres, associated with an inflammatory infiltrate of the myenteric plexus in idiopathic achalasia, provide evidence of an immune mediated destruction of the myenteric plexus, possibly through apoptotic process. This concept is reinforced by the concomitant appearance of achalasia and Guillain-Barré syndrome (GBS) and/or Parkinson's disease, where inappropriate initiation of apoptosis has been proposed to underlie the neuronal attrition. In the same respect, Helicobacter pylori (H. pylori) infection has been associated with gastric autoimmunity, and patients infected with H. pylori have been shown to possess autoantibodies that cross-react with antigens expressed on the gastric mucosa. Furthermore, H. pylori is thought to be associated with the development of autoimmune sequelae observed in peripheral neuropathies and GBS, where autoantibodies to specific neural targets have been found to impair native neural function by inducing nerve tissue damage, possibly by apoptosis. Taken together, we assume that H. pylori infection might be a pathogenetic factor of achalasia through induction of autoimmunity and apoptosis. Whether eradication of H. pylori infection may indirectly offer benefit to the pathophysiology of idiopathic achalasia by ameliorating the apoptotic loss of ganglion cells and their axons in the oesophageal wall remains to be elucidated.

Animals↗

PubMed1987

An immunohistochemical study of serotonin-containing nerves in the colon of rats.

The localization of the serotonin-like immunoreactive nerves of the rat colon was investigated by means of immunohistochemistry, utilizing an antibody against serotonin. In non-treated colons, serotonin-positive neuropils were consistently detected around the myenteric plexus. In pargyline-treated colons, serotonin-like fibres were demonstrated in association with either the small intramural blood vessels of the submucosa or the extramural nerve bundles. Treatment with 5-hydroxytryptophan (5-HTP) permitted the visualization of additional serotonin-immunoreactive fibres around the large extramural blood vessels. Immunoreactive nerve cell bodies were demonstrated in the myenteric plexus of colons treated with 5-HTP or colchicine. From these observations, it is suggested that the serotoninergic nerves of the rat colon comprise both intrinsic and extrinsic elements.

5-Hydroxytryptophan↗

PubMed2006

Atropine methyl nitrate increases myenteric but not dorsal vagal complex Fos-like immunoreactivity in the rat.

Atropine methyl nitrate (AMN, 0.05, 0.5 and 25 mg/kg) intraperitoneally increased Fos-like immunoreactivity (Fos-LI) in the myenteric plexus, but not the dorsal vagal complex (DVC, the area postrema (AP), nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus (DMV)) in adult, male Sprague-Dawley rats. A 3 mg/kg AMN dose decreased intake of 15% sucrose, but failed to increase Fos-LI in both locations. In conclusion, the myenteric plexus may play a local role in the behavioral response evoked by AMN.

Animals↗

PubMed2006

Multiple gastrointestinal stromal tumors of the ileum and neurofibromatosis type 1.

Type 1 neurofibromatosis, also known as von Recklinghausen disease, is one of the most common genetic disorders. Gastrointestinal associations have been well described in these patients, but the true incidence of gastrointestinal tumors and the proportion of these becoming clinically significant are not known. The most common gastrointestinal tumors are stromal tumors, most of which are located in the stomach and jejunum. We discuss the case of a female patient with neurofibromatosis whose initial diagnosis was an ovarian mass. During surgery the diagnosis of an intestinal stromal tumor was made. Operative findings were a multilobulated tumor arising from the ileal wall 50 cm from the ileocecal valve. The tumor did not originate from the nervous myenteric plexus or muscular layer of the small bowel wall; it originated from within the stromal cells of the intestinal wall. Mitotic count showed 3 mitoses per 10 high-power fields. Immunohistochemical stains of the tumor showed positive staining for CD117 and CD34 and negative staining for S100, alpha-smooth muscle actin, and desmin. The intestinal myenteric plexus showed positive staining for chromegranin A and S100. The histologic characteristics of this patient's tumor are compatible with an undifferentiated stromal tumor of nonneural or nonmuscular origin.

Adult↗

PubMed1992

Opioid enhancement of evoked [Met5]enkephalin release requires activation of cholinergic receptors: possible involvement of intracellular calcium.

Previous work from this laboratory has shown that the electrically evoked release of enkephalin from the guinea pig myenteric plexus is regulated by an opiate receptor-mediated, concentration-dependent mechanism. Low concentrations (nanomolar) of opioids enhance release, whereas higher concentrations (10-100 nM) inhibit release. Each opioid effect is mediated by a different guanine nucleotide-binding protein. We now demonstrate that activation of cholinergic receptors in the myenteric plexus is a prerequisite for opioid excitatory effects, but not inhibitory effects, on enkephalin release. Pretreatment with the muscarinic cholinergic receptor antagonist atropine abolishes the opioid facilitation of stimulated enkephalin release but does not alter the inhibition of release that is observed with higher concentrations of opioid agonist. Exposure to the calcium ionophore A23187 overcomes the abolishment of opioid enhancement of enkephalin release produced by cholinergic receptor blockade. In tissue treated with both atropine and A23187, the magnitude of the opioid enhancement of release is indistinguishable from that observed in untreated preparations. This suggests that the lack of stimulation-induced generation of elevated cytosolic calcium is responsible for the abolishment of facilitory opioid effects when cholinergic receptors are blocked. The known coupling of muscarinic receptors to phospholipase C activation and the generation of inositol trisphosphate (which elevates cytosolic calcium) could suggest that this second messenger is critical for the manifestation of opioid facilitation of enkephalin release.

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

PubMed1995

Effect of nitroblue tetrazolium on NO synthase and motor function of opossum esophagus.

Nitric oxide mediates neuromuscular events in the opossum esophagus. The NADPH diaphorase stain is used to localize nitric oxide synthase-containing enteric neurons. Cells stain by the NADPH diaphorase technique because they reduce nitroblue tetrazolium to the visible formazan. The effects of nitroblue tetrazolium on neuromuscular function and nitric oxide synthase of esophageal muscle were studied. The NADPH diaphorase stain was performed. Nitroblue tetrazolium inhibited lower esophageal sphincter relaxation, abolished the latency gradient of the off response, and inhibited nitric oxide synthase. The NADPH diaphorase technique stained myenteric plexus nerve cell bodies and nerve processes. Nitroblue tetrazolium is not a nonspecific muscle or nerve toxin, as nerve-mediated cholinergic responses, responses to exogenous nitric oxide, and responses to myogenic stimulation were maintained after nitroblue tetrazolium abolished the off response and lower esophageal sphincter relaxation. Nitroblue tetrazolium inhibits nitric oxide-mediated events and nitric oxide synthase. It stains neurons in the esophageal myenteric plexus.

Animals↗

PubMed2004

Dextran sodium sulfate-induced colitis reveals nicotinic modulation of ion transport via iNOS-derived NO.

In normal colon, ACh elicits a luminally directed Cl- efflux from enterocytes via activation of muscarinic receptors. In contrast, in the murine model of dextran sodium sulfate (DSS)-induced colitis, an inhibitory cholinergic ion transport event due to nicotinic receptor activation has been identified. The absence of nicotinic receptors on enteric epithelia and the ability of nitric oxide (NO) to modulate ion transport led us to hypothesize that NO mediated the cholinergic nicotinic receptor-induced changes in ion transport. Midportions of colon from control and DSS-treated mice were examined for inducible NO synthase (iNOS) expression by RT-PCR and immunofluorescence or mounted in Ussing chambers for assessment of cholinergic-evoked changes in ion transport (i.e., short-circuit current) with or without pretreatment with pharmacological inhibitors of NO production. iNOS mRNA and protein levels were increased throughout the tissue from DSS-treated mice and, notably, in the myenteric plexus, where the majority of iNOS immunoreactivity colocalized with the enteric glial cell marker glial fibrillary acidic protein. The drop in short-circuit current evoked by the cholinomimetic carbachol in tissue from DSS-treated mice was prevented by selective inhibitors of iNOS activity [N6-(1-iminoethyl)-lysine HCl and N-[3-(aminomethyl)benzyl]acetamidine] or an NO scavenger [2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide] or by removal of the myenteric plexus. Thus, in this model of colitis, a "switch" occurs from muscarinic to nicotinic receptor-dominated control of cholinergic ion transport. The data indicate a novel pathway involving activation of nicotinic receptors on myenteric neurons, resulting in release of NO from neurons or enteric glia and, ultimately, a dampening of stimulated epithelial Cl- secretion that would reduce secretory diarrhea.

Animals↗

PubMed1996

Morphological analysis of vagal input to gastrin releasing peptide and vasoactive intestinal peptide containing neurons in the rat glandular stomach.

Vagal preganglionic efferents to the rat stomach were labeled anterogradely by injecting the fluorescent carbocyanine dye DiA into the dorsal motor nucleus in vivo. Enteric neurons were labeled in toto by intraperitioneal administration of Fluorogold, and neurochemically characterized by simultaneous single- and double-label immunocytochemistry. Single peptide immunocytochemistry revealed that in all three major areas of the stomach, about one-third of all gastrin-releasing peptide immunoreactive (GRP-IR) neurons in the myenteric plexus, received vagal contacts. Because the proportion of GRP-IR neurons was 32% in the fundus, 23% in the corpus, and only 8% in the antrum, the absolute number of vagally contacted GRP-IR neurons per cm2 was also different. Double-label immunocytochemistry revealed colocalization of vasoactive intestinal peptide immunoreactivity (VIP-IR) in 45%, and of enkephalin immunoreactivity (ENK-IR) in about 30%, of the GRP-IR myenteric neurons. A subpopulation of myenteric neurons colocalized GRP-IR and VIP-IR and projects almost exclusively to the gastrin cell-rich basal mucosa of the antrum and the oxyntic mucosa of the corpus. Another subpopulation containing GRP-IR, but not VIP-IR, projects mainly to the myenteric plexus itself and the external muscle layers, particularly the longitudinal muscle. A third group of neurons containing VIP-IR but not GRP-IR projects heavily to the circular muscle layer, the muscularis mucosae, and to other myenteric neurons. Vagal input to these three subpopulations seems not to be selective, in that an equal proportion of about 20 to 30% of each group was vagally contacted. Vagal inputs to these neurochemically and topographically distinct enteric neurons provide the basis for the physiological vagal control of gastrin release, gastric acid secretion, and gastric motility.

Animals↗

PubMed2005

Diabetes only affects nitric oxide synthase-containing myenteric neurons that do not contain heme oxygenase 2.

It has been demonstrated that subpopulations of myenteric neurons are differentially susceptible to the development of neuropathy in diabetes. Within the myenteric plexus are neurons that contain neuronal nitric oxide synthase (nNOS). However, these are not a homogeneous population. Some of the nNOS-containing neurons also contain heme oxygenase 2 (HO2). Therefore, the aim of this study was to compare the effects of diabetes on HO2- and nNOS-containing neurons within the myenteric plexus of the rat ileum. Diabetes was induced in male Wistar rats (350-400 g) by a single i.p. injection of buffered streptozotocin (65 mg/kg). After 12 weeks, immunostaining of wholemount preparations of ileum revealed that diabetes induced a significant shift (P < 0.001, chi-squared test for trend) towards increased neuronal cell body size in nNOS-immunoreactive neurons while HO2-immunoreactive neurons remained unaffected. Double-labeling studies revealed that approximately 50% of nNOS-containing neurons also contained HO2 and that the diabetes-induced change in size was confined to nNOS-immunoreactive neurons that did not contain HO2 (P < 0.01). No change in the size distribution occurred in neurons in which nNOS and HO2 were colocalized. Differences in the response of these two subpopulations of nNOS-containing neurons to diabetes could occur because they supply different targets within the gastrointestinal tract or indicate that the antioxidant, HO2, protects those nNOS-containing neurons in which it is colocalized, against oxidative stress that occurs in diabetes.

Animals↗

PubMed2002

Sympathetic denervation-induced changes in G protein expression in enteric neurons of the guinea pig colon.

Chronic sympathetic denervation entails subsensitivity to alpha(2)-adrenoceptor agonists and supersensitivity to kappa- and mu-opioid receptor agonists modulating cholinergic neurons in the guinea pig colon. A possible role for signal transduction G proteins in contributing to development of these sensitivity changes was investigated. Pertussis toxin (PTX), a blocker of the G(i/o)-type family of G proteins significantly reduced the inhibitory effects of UK14,304 (alpha(2)-adrenoceptor agonist), U69593 (kappa-opioid receptor agonist) and DAMGO (mu-opioid receptor agonist) on acetylcholine (ACh) overflow in preparations obtained from normal animals, but not in those obtained from sympathetically denervated animals. In this experimental condition, immunoblot analysis revealed reduced levels of G(alphao), G(alphai2), G(alphai3) and G(beta) in myenteric plexus synaptosomes. On reverse, synaptosomal levels of G(alphai1) and G(alphaz), a PTX-insensitive G-protein, increased after chronic ablation of the sympathetic pathways. These data suggest that changes in the function and expression of inhibitory G proteins coupled to alpha(2)-adrenoceptors, kappa- and mu-opioid receptors occur in the myenteric plexus of the guinea pig colon after chronic sympathetic denervation. The possibility that regulation of G proteins represents one of the biochemical mechanisms at the basis of the changes in sensitivity of enteric cholinergic neurons to alpha(2)-adrenoceptor, kappa- and mu-opioid receptor agonists is discussed.

Acetylcholine↗

PubMed2004

Cyclooxygenase-2 contributes to dysmotility and enhanced excitability of myenteric AH neurones in the inflamed guinea pig distal colon.

We have previously demonstrated that trinitrobenzene sulphonic acid (TNBS)-induced colitis in guinea pig is associated with hyperexcitability of myenteric AH neurones, enhanced synaptic activity in the myenteric plexus, increased serotonin (5-HT) availability in the mucosa, and decreased propulsive motor activity. The current study tested the hypothesis that the activation of cyclooxygenase (COX) contributes to these alterations in bowel functions. DFU inhibition of COX-2, but not SC-560 inhibition of COX-1, restored to normal levels the electrical properties of myenteric AH neurones, the proportion of S neurones exhibiting slow EPSPs, and the rate of propulsive motor activity. Neither inhibitor was effective in altering the level of inflammation, the increased availability of mucosal 5-HT, or the enhanced fast EPSPs in myenteric AH and S neurones. COX-2 expression is enhanced in the myenteric plexus and cells within the smooth muscle layers during colitis, possibly reflecting the site at which COX-2 inhibition acts to allow recovery of motor function. In support of this concept, COX-1, but not COX-2, inhibition was effective in restoring normal mucosal prostaglandin levels. These results indicate that the various changes that occur in the motor neural pathways of the distal colon in TNBS-induced colitis do not involve a single neuroimmune mechanism. COX-2 activation is a critical step in the enhanced excitability of AH neurones as well as diminished propulsive motility in TNBS colitis, whereas other yet to be resolved pathways, that do not involve COX-1 or COX-2 activation, lead to altered 5-HT content in the mucosa and an augmentation of fast EPSPs.

Animals↗

PubMed1989

Sennosides do not kill myenteric neurons in the colon of the rat or mouse.

Effects of senna on the myenteric plexus of the colon were investigated in view of earlier reports that this anthraquinone cathartic depletes the plexus of its intrinsic neurons. Rats and mice were given purgative doses of sennosides in their drinking water for 4 and 5 months, respectively. Body growth was reduced, and the weight of the colon with its contents was increased relative to the weight of the whole body in the treated animals. The latter change was attributed to depressed propulsive motility of the large intestine. Total numbers of myenteric neurons were determined from whole-mount preparations stained with Cuprolinic Blue-magnesium chloride, which selectively coloured the neuronal somata. The number of neurons in the rat's colon was unaffected by treatment with senna, but the colons of the treated mice contained significantly more neurons than those of their controls. Staining with antisera to 10 putative neurotransmitters or their associated enzymes revealed immunoreactive somata and axons in the myenteric plexus. Treatment with senna was not associated with absence of neuronal somata or fibres stainable with any of the antisera in either species. Thus, there was no evidence of toxic destruction of any identifiable population of neurons that might have been too small to affect the total counts. We conclude that senna does not kill myenteric neurons in the colon of the rat or mouse.

Administration, Oral↗

PubMed1987

Effects of three mammalian tachykinins on single enteric neurons.

The effects of substance P (SP), substance K (SK) and neuromedin K (NMK) were compared on single neurons of the guinea pig myenteric plexus. The tachykinins depolarized all myenteric neurons with a rank order of potency SP greater than SK greater than NMK. In approximately 80% of neurons studies the depolarization was associated with an increase in membrane resistance: in 20% membrane resistance decreased. The depolarizations were not affected by tetrodotoxin (TTX) (300 nM), hyoscine (1 microM) or by [D-Arg1, D-Pro2, D-Trp7,9, Leu11]SP (1 microM). These results provide no evidence for more than one type of tachykinin receptor on myenteric neurons.

Animals↗

PubMed1995

The selective beneficial effects of nitric oxide inhibition in experimental colitis.

We investigated the involvement of nitric oxide in trinitrobenzene-sulfonic acid (TNB) colitis. Every 24 h after TNB, rats were orally dosed with NG-nitro-L-arginine methyl ester (L-NAME; 30 mg/kg), NG-nitro-D-arginine methyl ester (D-NAME), or water, and food intake, body weight, and plasma nitrite levels were measured. On day 6, colonic nitric oxide synthase and myeloperoxidase (MPO) activity, histology, intestinal muscle growth, NADPH-diaphorase, and myenteric nerve function were assessed. Food intake and body weight were reduced during the first 72 h of colitis. On day 6 post-TNB, a fourfold increase in mucosal nitric oxide synthase, a 30-fold increase in MPO, and a fivefold elevation in plasma nitrite were measured. Smooth muscle hyperplasia and hypertrophy in both colonic muscle layers, numerous diaphorase-positive macrophages in the myenteric plexus, and a suppression of myenteric nerve function were also observed. Unlike D-NAME, oral L-NAME reduced MPO and intestinal muscle hyperplasia by > 90%. Likewise, plasma nitrite and colonic nitric oxide synthase were reduced by > 70%. L-NAME completely prevented macrophage infiltration into the muscle. Conversely, it had no effect on anorexia or intestinal smooth muscle hypertrophy, nor did it affect suppressed myenteric nerve neurotransmitter release. These results demonstrate the selective transmural protective effects of L-NAME in the inflamed colon, implicating nitric oxide as a mediator.

Amino Acid Oxidoreductases↗

PubMed1997

Effects of mercuric chloride and methyl mercury on cholinergic neuromuscular transmission in the guinea-pig ileum.

The effects of mercuric chloride (HgCl2) and methyl mercury (MeHg) were examined on basal mechanical activity and electrically-induced neurogenic cholinergic contractions (twitch contractions) in longitudinal muscle-myenteric plexus strips from guinea-pig distal ileum. Both compounds at 0.33 microM slightly enhanced the amplitude of twitch contractions in approximately 50% preparations. This effect was probably due to facilitation of acetylcholine (ACh) release since 0.1 and 1 microM mercurials increased electrically-evoked tritium outflow from [3H]choline preloaded muscle layer with attached myenteric plexus. Conversely, higher mercury concentrations inhibited twitch contractions (HgCl2 IC50 = 21.3 +/- 6.4 microM; MeHg IC50 = 45.1 +/- 5.5 microM), as well as contractions to exogenous ACh (0.1 microM) in resting preparations, and concomitantly increased the basal tone. The former effects possibly reflected an antimuscarinic activity of mercury, while the latter was related to alterations of calcium homeostasis in the effector cells. Indeed, the effect of HgCl2 on basal tone was antagonized by the Ca2+ entry blocker nifedipine (3, 10, 30 nM), indicating Hg-induced facilitation of Ca2+ influx through voltage-dependent channels. On the whole, our results suggest that cholinergic neuromuscular transmission and Ca(2+)-dependent mechanisms underlying smooth muscle contractility are targets for mercury toxicity in the intestine.

Acetylcholine↗

PubMed1983

Distribution and projections of nerves with enkephalin-like immunoreactivity in the guinea-pig small intestine.

Whole mounts of guinea-pig small intestine were used to examine the distribution of neurons with enkephalin-like immunoreactivity and the effects of microsurgical lesions on these neurons. The enkephalin neurons are intrinsic to the intestine. Cell bodies are found in the myenteric ganglia; processes are in the myenteric plexus, circular muscle (including deep muscular plexus) and submucosa, but not in the mucosa. The cell bodies have one prominent process and several short processes, the latter occasionally are seen to give rise in turn to fine, faint processes. The prominent processes provide fibres to the circular muscle and deep muscular plexus beneath and just anal (up to about 2 mm) to the cell bodies. Fibres in the submucous ganglia come from the overlying myenteric plexus. Orally-directed processes (possibly dendrites) of myenteric cell bodies provide the varicose fibres in the myenteric ganglia. These processes are 3.5-4 mm long. The enkephalin neurons represent a population of enteric neurons, with a distinct distribution and projections, which does not correspond to any of the other populations of enteric neurons that have been studied.

Animals↗