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PubMed1980

[Paralysis of digestive tract with lesions of myenteric plexuses. A new paraneoplastic syndrome (author's transl)].

A 67 years old man was admitted on July 1979 for nausea, dysphagia and rectal pain. At age 64 he had undergone radiotherapy on the lower lip for an epidermoid carcinoma. He remained then healthy. His medical history was negative with the exception of chronic bronchitis. He had never been exposed to toxic agents or drugs and had never left Europe. A few days after admission he suffered acute intestinal obstruction but at laparostomy no etiology was found. At the same time the patient complained of pain in all four limbs and he was found to have diffuse wasting of muscles, areflexia and distal sensory loss. No sign of dysautonomia was present. Physical examination was negative with the exception of a cervical lymphadenopathy. The lymph node biopsy showed an undifferentiated metastatic carcinoma. Negative investigations included: blood cells count; serum ionogram and immunoelectrophoresis; thyroid function tests; serological test for Chagas' disease. The following abnormalities were found: ESR: 55-105; CSF protein: 145 mg/100 ml and 1 cell mm3; whole blood folic acid: 1,7 mg/ml; Hbs antigen was present in blood; EMG showed evidence of denervation but motor conduction velocities were normal. By September the patient's weakness had increased and complete intestinal obstruction persisted. At oesophageal, gastric and duodenal fibroscopy no contraction was visible, and biopsies were negative. The patient died of peritonitis on October 5th, 1979. At necropsy peritonitis secondary to multiple perforation of the large bowel was found. No recurrence of the lip carcinoma or metastase or evidence of a primary carcinoma was found. Light microscopy showed no evidence of amyloidosis or scleroderma. Examination of the alimentary tract showed abnormalities restricted to the myenteric plexuses which varied from one level to another. In the small bowel there was hyperplasia of the smooth muscle and the myenteric plexuses were enlarged by marked proliferation of Schwann cells. Severe neuronal loss and nodules of Nageotte were also noted. Schwann cells proliferation was less marked in the stomach and large bowel. Lympho-histiocytic infiltration strictly confined to the region of the myenteric plexuses was present in oesophagus, stomach, large bowel and rectum. Mild chronic inflammatory lesions were also found in anterior and posterior spinal roots and semi-lunar ganglia. The striking feature of this case is the association of an undifferentiated carcinoma and a polyradiculoneuritis with a complete alimentary tract palsy of rapid onset, secondary to lesions restricted to the myenteric plexuses. The low folate level was insufficient to explain the neuropathy. Investigations showed no evidence of the usual causes of intestinal pseudo-obstruction: muscular, dysautonomic, toxic, plexic (idiopathic, familial, inflammatory), Chagas' disease). The clinical course, the pathological pictures of the alimentary tract and spinal roots and the association with a carcinoma suggest that our case may represent a paraneoplastic syndrome...

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PubMed1989

Myenteric plexus of frog large intestine: light and electron microscopy of fiber system and neurons.

The myenteric plexus of the frog large intestine was studied by means of silver impregnation, NADH-diaphorase histochemistry and electron microscopy. The main fiber bundles of the myenteric plexus are situated between the longitudinal and circular smooth muscle layers. Most of the branches of this main plexus could be followed into the circular muscle layer. The diameter of the large nerve bundles was demonstrated by impregnation to be 7-8 microns. NADH-diaphorase histochemistry revealed a random distribution of the nerve cells; the nerve cells did not form ganglia. The maximal profile of these mostly multipolar cells was 75-100 microns 2. The packing density of nerve cells was 710 +/- 23 per cm2. At the electron microscopic level, the plexus consisted of a number of unmyelinated nerve profiles, a few myelinated axons, Schwann cells and neurons. The proportion of myelinated fibers did not exceed 1%. The nerve profiles contained vesicles, small agranular vesicles or mixed vesicle populations. Synapses were extremely rare in the neuropil. The possibility and importance of non-synaptic transmitter release and presumed transmitter substances are discussed.

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PubMed1986

The presence of extraganglionic fluorescent neurons in the myenteric plexus of the guinea pig small intestine.

Fluorescent histochemical observations of the small intestine of the guinea pig demonstrated that single fluorescent cell bodies, separate from the ganglia, were present in the myenteric plexus. These cell bodies gave rise to single processes which entered the ganglia or the interganglionic strands. They were of a very small size, and the intensity of their fluorescence increased by pretreatment with L-DOPA and nialamide. Interruption of extrinsic nerve pathways to the small intestine caused a disappearance of the meshwork of fluorescent fibers in the myenteric plexus; but in some areas a fluorescent fiber which supplied its terminal to the ganglion was seen to remain. A photograph taken from the denervated myenteric plexus revealed that a long process arising from an extraganglionic cell entered the ganglion and ramified into terminal branches.

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PubMed1978

Factors influencing the release of acetylcholine from the myenteric plexus of the ileum of the guinea-pig and rabbit.

1 The effects of electrical stimulation, changes in external ion concentrations and various drugs on acetylcholine release from the myenteric plexus were measured by bioassay in the presence of physostigmine and by recording the responses of the longitudinal muscle. In preparations from the guinea-pig, the acetylcholine output per pulse increased with decreasing frequency of stimulation and reached its maximum at a frequency of 0.017 Hz (1/min) and thus ensured that the output per unit of time was constant at frequencies below 0.5 Hz. Spontaneous release was suppressed during stimulation at 0.017 Hz. 2 In the rabbit, the fractional acetylcholine release was lower than in the guinea-pig. The output per pulse increased with decreasing frequency of stimulation but at a lesser rate, with the effect that the output per unit decreased between 0.5 and 0.017 Hz. 3 In the guinea-pig, reduction of the Ca2+ concentration, addition to the bath fluid of Mn2+, ganglion-blocking drugs, morphine and catecholamines reduced output more at low than at high frequencies of stimulation. In the rabbit, acetylcholine output was less sensitive to changes in Ca2+ concentration and insensitive to Mn2+ and morphine. 4 In the guinea-pig, morphine and catecholamines depressed both the contractile response and acetylcholine output whereas Mn2+ in concentrations up to 125 muM, bretylium and ganglion-blocking drugs depressed only acetylcholine output. 5 In preparations from the guinea-pig, drugs blocking noradrenergic neurons or alpha-adrenoceptors, e.g. bretylium, phenoxybenzamine, thymoxamine and phentolamine, increased acetylcholine output during stimulation at high (1.5 to 10 Hz) but not at low frequencies. 6 The implications of these findings for the release of acetylcholine from different pools in the heterogeneous myenteric plexus are considered. The possible errors, introduced by the effects of physostigmine, on the size of the acetylcholine pools and on the transmission of impulses within the myenteric plexus are discussed.

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PubMed2001

Myenteric plexus of obese diabetic mice (an animal model of human type 2 diabetes).

The myenteric plexus of the gastrointestinal tract was investigated in the obese diabetic mouse, an animal model of human type 2 diabetes. Sections were immunostained by the avidin-biotin complex method, using a general nerve marker, protein gene product 9.5 (PGP 9.5), as well as antibodies to several important neurotransmitters. Computerized image analysis was used for quantification. When diabetic mice were compared with controls, no difference was found in the density of PGP 9.5-immunoreactive (IR) nerve fibres in antrum, duodenum or colon. In antrum and duodenum, diabetic mice showed a decreased number of vasoactive intestinal peptide (VIP)-IR neurons in myenteric ganglia as well a decreased relative volume density in myenteric plexus (though not significantly in antrum, p=0.073). No difference was found regarding VIP-IR nerves in colon. The volume density of nitric oxide synthase (NOS)-IR nerve fibres was decreased in antrum and duodenum of diabetic mice, whereas no difference was found in colon. The density of galanin-IR nerve fibres was decreased in duodenum. Whereas neuropeptide Y (NPY)- and vesicular acetylcholine transporter (VAChT)-IR nerve fibres was increased in density in colon of diabetic mice, no difference was found in antrum and duodenum. Regarding substance P, there was no difference between diabetic and control mice in antrum, duodenum or colon. The present study shows that gut innervation is affected in this animal model of human type 2 diabetes. It is possible that the present findings may have some relevance for the gastrointestinal dysfunctions seen in patients with type 2 diabetes.

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PubMed2006

Effect of change in an inhibitory neurotransmitter of the myenteric plexus on the pathogenetic mechanism of irritable bowel syndrome subgroups in rat models.

OBJECTIVE: In order to investigate the effect of change in an inhibitory neurotransmitter of the myenteric plexus on irritable bowel syndrome (IBS) subgroups, the amounts of nitric oxide (NO) in constipation-predominant (C-IBS) and diarrhea-predominant (D-IBS) IBS models in rats were studied. METHODS: The D-IBS model was created in rats by intracolonic instillation of acetic acid and by restraint stress. The D-IBS control group underwent intracolonic instillation with saline instead. The C-IBS model was created in rats by gastric instillation of 0-4 degrees C cool water daily for 14 days. The C-IBS control group underwent gastric instillation with saline instead. A blank control group was also made. Viscerosomatic sensitivity was assessed with electromyographic (EMG). Abdominal contractions induced by distension of a colonically inserted balloon (0-1.6 mL) was recorded in rats by implanting electrodes in the abdominal external oblique muscle. An India ink gastric instillation experiment was used to detect the bowel movement and fecal pellets formation. Histological analysis of colonic tissue was performed. Nicotinamide dinucleotide phosphate (NADPH)-diaphorase staining was used to detect positive NO neurons in the myenteric plexus. RESULTS: When the balloon was distended by high volume, there were significantly more contractions of abdominal muscle in D-IBS compared with C-IBS and the control groups (P < 0.05). When the balloon was distended by low volume, there were significantly fewer contractions of abdominal muscle in C-IBS compared with D-IBS and the control groups (P < 0.05). The wet weight and water content of the feces expelled by the rats in the C-IBS and the C-IBS control groups were significantly lower than those in the blank control group (P < 0.05). The time before the first black stool in the C-IBS group was significantly longer than that in the blank control group and C-IBS control group (P < 0.05). Histological analysis of the colon showed no colonic inflammation in any group. The number of NO-positive neurons in the C-IBS group was significantly greater than in the D-IBS and control groups (P < 0.01), although there was no significant difference in the number of neurons between the D-IBS and the control groups (P > 0.05). CONCLUSIONS: Enhanced inhibitory neurotransmitter NO in the myenteric plexus of the colon is related to IBS subgroups, visceral sensitivity and motility dysfunction. The results reveal that NO plays a role in the pathogenetic mechanism of IBS subgroups.

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PubMed1986

Opiates induce long-term increases in prodynorphin-derived peptide levels in the guinea-pig myenteric plexus.

The subcutaneous administration of a single dose of an opiate agonist (levorphanol) or antagonist (naloxone) to guinea pigs results in an at least 3-fold elevation of dynorphin and alpha-neoendorphin-immunoreactivity in the longitudinal muscle myenteric plexus preparation. The effects are time- and dose-dependent, significant elevations first being observed 6 h after treatment and lasting for up to 24 h. Pretreatment levels of opioid peptides were observed after 8 days. Combined injection of the narcotic agonist and antagonist, at sufficiently high doses, resulted in an additive effect of the individual drugs. The respective stereoisomers dextrorphan and (+)-naloxone did not affect prodynorphin-derived peptide concentrations. An increase of endogenous opioids was also observed after administration of the nonopiate clonidine, a compound which, like opiates, alters the activity of the myenteric plexus. It is suggested that feedback mechanisms in the myenteric plexus are responsible for the elevation of endogenous opioid peptides following exposure to exogenous opiates. Using a monoclonal antibody (3-E7), which recognizes virtually all endogenous opioid peptides, it was found that levels of higher molecular material were also increased upon opiate challenge. This suggests that a single dose of an exogenous opiate results in an increase in peptide synthesis.

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PubMed1985

[Myenteric plexuses and colonic diverticulosis: results of a histological study].

The implication of intraluminal hyperpressure in the pathogenesis of colonic diverticulosis was investigated. Since colonic motricity depends on the anatomical integrity of the myenteric plexuses, we looked for morphological abnormalities of these plexuses in diverticulosis of the sigmoid, using the silver impregnation technique devised by Smith. Fifteen sigmoidectomy specimens (including the rectosigmoid junction) were studied in patients afflicted with diverticulosis. Operations were not performed during the acute phases of the illness. The results were compared to those obtained in 5 colectomy specimens in patients with cancer of the rectum, without colonic diverticulosis (control series). Conventional histology as well as the silver impregnation did not reveal any morphological abnormalities of the myenteric plexuses in the rectosigmoid junction or in the remaining sigmoid. The count of argyrophilic ganglion cells (10 to 15 per plexus) was identical in the colons affected with diverticulosis and in the control specimens. These results show that impairment of motricity in sigmoid diverticulosis is not a consequence of morphological abnormalities of the myenteric plexuses. They do not, however, exclude chemical or functional modifications in these plexuses.

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PubMed1991

Distribution of argininosuccinate synthetase-like immunoreactive neurons in the rat myenteric plexus: a whole mount study.

The distribution of argininosuccinate synthetase (ASS)-like immunoreactive neurons in the myenteric plexus of the rat alimentary tract were immunocytochemically studied using whole-mount tissues. The present study revealed ASS-like immunoreactive meshworks of ganglia and interconnecting nerve strands in the myenteric plexus of almost all parts of the alimentary tract. ASS-like immunoreactive neurons constituted about 11% of the myenteric cell.

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PubMed1991

Relationship between appearance of GABA, fluorogenic monoamines and cytochrome oxidase activity during prenatal morphogenesis of chick myenteric plexus.

The basic histology of the developing embryonic gut wall of the chick was examined on haematein and eosin-stained paraffin sections. In parallel with this, the ontogenic sequence of myenteric plexus formation was followed on whole mounts after NADH diaphorase histochemistry. The presence of nerve elements was verified also by electron microscopy. The appearance of enteric gamma-aminobutyric acid-containing neurons, as an example of an intrinsic inhibitory neuronal system, was studied by using an antiserum against the gamma-aminobutyric acid glutaraldehyde bovine serum albumin conjugate. The development of noradrenergic innervation as an extrinsic inhibitory supply was followed by means of a glyoxylic acid-induced fluorescence method. Cytochrome oxidase activity was detected histochemically. Three consecutive steps of the morphogenesis of the myenteric plexus were revealed; first the appearance of a cellular crest at the mesenteric border on embryonic day 9; second the migration and clustering of nerve cells between embryonic days 10 and 16; then the elongation of neurites on embryonic days 16 and 21. Immunoreactive and also fluorescent fibres were first detected on the 14th day of incubation, while immunopositive cell bodies appeared only after hatching. In the early stages the cytochrome oxidase activity was restricted to the perikarya, while at the end of embryonic development the activity also appeared in the ganglionic neuropile. On the basis of these observations, we concluded that there is a close time relation between the morphogenesis and the biochemical and functional maturation of the myenteric plexus.

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PubMed1981

Slow synaptic potentials in AH-type myenteric plexus neurons.

Two types of slow depolarization were recorded in AH-type guinea pig myenteric plexus neurons when the myenteric plexus-longitudinal muscle preparation was stimulated transmurally with external electrodes. One depolarization was associated with a fall and the other with a rise in membrane resistance, the latter type (slow EPSP) being encountered about six times more commonly than the former. In some instances both types of potential were recorded in the same AH neuron. When this occurred the amplitude and duration of the slow EPSP was attenuated if it was timed to occur at about the same time as the other slow synaptic potential.

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PubMed1986

The effect of ascorbate on the acetylcholine release from guinea-pig ileal myenteric plexus.

The effect of ascorbate on the release of acetylcholine from the longitudinal muscle-myenteric plexus preparation of the guinea-pig isolated ileum has been investigated using a bioassay and an isotopic technique. Ascorbate at 5 mM increased the spontaneous output of acetylcholine and enhanced DMPP-induced output of acetylcholine, while iso-ascorbate, 5 mM, did not. Ascorbate did not influence either the spontaneous or the DMPP-induced release of acetylcholine from synaptosomes of the ileal myenteric plexus. These results suggest that ascorbate promotes acetylcholine release from intramural cholinergic nerves.

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PubMed1989

Image analysis of the sympathetic innervation of the myenteric plexus in the small intestine of mammalian species.

1. The arrangement of the sympathetic innervation of the myenteric plexus varies between mammalian species. 2. In larger mammals the density of sympathetic innervation of the myenteric plexus is significantly less than in small (less then 1 kg) species. 3. The number of varicosities on the terminal parts of sympathetic neurons innervating the gut is significantly less in larger mammals.

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PubMed2003

Signalling mechanism coupled to 5-hydroxytryptamine4 receptor-mediated facilitation of fast synaptic transmission in the guinea-pig ileum myenteric plexus.

5-hydroxytryptamine (HT)4 receptor agonists stimulate gastrointestinal motility partly by facilitating acetylcholine release from myenteric neurones. However, the signalling mechanisms that couple 5-HT4 receptor activation to increased transmitter release in the myenteric plexus are unknown. We used conventional intracellular electrophysiological methods to record fast excitatory postsynaptic potentials (fEPSPs) from neurones in the guinea-pig ileum myenteric plexus preparation. The substituted benzamide, renzapride, acted at 5-HT4 receptors to facilitate fEPSPs. This response was mimicked by forskolin, an activator of adenylate cyclase. Facilitation of fEPSPs by renzapride and forskolin was not blocked by treating tissues with pertussis toxin (PTX) (2 h, 2 microg mL-1). Facilitation of fEPSPs caused by renzapride was blocked by the non-selective protein kinase inhibitors, staurosporine (1 micromol L-1) and H-8 (30 micromol L-1) and by the selective protein kinase A (PKA) inhibitor, H-89 (10 micromol L-1). These data indicate that 5-HT4 receptors act via a PTX-resistant mechanism to activate PKA. Protein kinase A activation leads to an increase in transmitter release from myenteric nerve terminals and a facilitation of fast excitatory synaptic transmission.

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PubMed1988

Intracellular recordings from cells in the myenteric plexus of the rat duodenum.

Intracellular recordings were made in vitro from neurons in the myenteric plexus of freshly dissected preparations of the duodenum of the rat. Nearly one-quarter of neurons (18 out of 77) had long after-hyperpolarizations following their action potentials. Over 60% of neurons (20 out of 32) which were tested exhaustively by focal stimulation at seven points around the recording site were seen to receive fast excitatory synaptic inputs. These were of very short duration (10-30 ms) and were reversibly blocked by the nicotinic antagonist hexamethonium. Only four out of 18 after-hyperpolarization cells (22%) had visible fast synaptic inputs. Seven out of 32 neurons tested received slow excitatory synaptic inputs lasting up to 60 s that were associated with a decrease in conductance and an increase in excitability. No evidence for muscarinic synaptic potentials was seen; only four cells out of 30 with fast excitatory postsynaptic potentials had slow excitatory synaptic potentials visible after a single-shot stimulus; in none of these were the slow excitatory postsynaptic potentials blocked by atropine (up to 1 x 10(-5) M). No inhibitory postsynaptic potentials were recorded in any of the 77 neurons recorded in this study. The effects of five neurotransmitter candidates (acetylcholine, GABA noradrenaline, 5-hydroxytryptamine and substance P) applied by pressure microejection were studied. It is concluded that most of the neurophysiological features reported in the extensively studied guinea-pig small bowel myenteric plexus are present in the rat duodenum. However, the apparent lack of muscarinic synaptic potentials and inhibitory synaptic potentials suggests that there may be some differences between the two species. Our recordings also differ slightly from recently reported studies of rat myenteric neurons grown in cell culture.

Acetylcholine↗

PubMedDate not supplied

Density distribution of guinea pig myenteric plexus nerve endings containing immunoreactive substance P.

The present study was performed to investigate how myenteric plexus nerve endings containing substance P are distributed in sucrose density gradients in relation to nerve endings capable of taking up 3H-acetylcholine or 14C-noradrenaline. The peak of substance P-immunoreactivity (ISP) was found at a density of 1.157 +/- 0.001 g X ml-1, that of 3H-radioactivity at 1.160 +/- 0.002 and that of 14C-radioactivity at 1.162 +/- 0.002 g X ml-1 (mean +/- SEM, N = 6); there was considerable overlap. In a second set of experiments, the resuspended P2-pellet was layered upon a discontinuous density gradient consisting of 0.6, 1.0, 1.2 and 1.4 M sucrose. Nine fractions were recovered. There was a 2.5-3.4-fold increase in the relative specific activity of ISP in the 1.2 M fraction (density = 1.154 g X ml-1) and the adjoining interfaces. Conventional electron microscopy showed that synaptosomal elements were present in the transmitter-enriched fractions. It is concluded that the substance P-containing nerve endings of the guinea pig myenteric plexus co-distribute (and may be co-purified with) nerve endings utilizing noradrenaline or acetylcholine on sucrose density gradients.

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PubMed1994

Synergism between interleukins 1 beta and 6 on noradrenergic nerves in rat myenteric plexus.

BACKGROUND/AIMS: Because levels of interleukins 1 beta and 6 (IL-1 beta and IL-6) are elevated during intestinal Trichinella spiralis infection, they may mediate the changes in enteric neural function in that model. IL-1 beta suppresses norepinephrine release from the myenteric plexus, but the effect of IL-6 is unknown. Therefore, we investigated the effects of IL-6 alone and in combination with IL-1 beta on norepinephrine release. METHODS: Longitudinal muscle myenteric plexus or myenteric nerve varicosity preparations from jejunum of noninfected rats were loaded with [3H]norepinephrine, and 3H release was measured after a preincubation with or without human recombinant IL-6, alone or in combination with human recombinant IL-1 beta. RESULTS: 1 ng/mL of IL-6 augmented 3H release, 100 ng/mL suppressed 3H release, whereas 10 ng/mL had no effect. However, IL-6 (10 ng/mL) plus a subthreshold concentration of human recombinant IL-1 beta significantly suppressed 3H release, and this was abolished by adding anti-IL-6 antibody or an IL-1 receptor antagonist. CONCLUSIONS: Because 3H release reflects [3H]norepinephrine release, our results show that IL-6 exerts a dual effect on norepinephrine release. Furthermore, there is synergism between IL-1 beta and IL-6 resulting in suppression of norepinephrine release. Therefore, both cytokines may contribute to the suppression of norepinephrine release observed in the inflamed intestine.

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PubMed1990

Mechanisms regulating somatostatin release and somatostatin-induced acetylcholine release from the myenteric plexus.

The present studies were performed to characterize the molecular form(s) of somatostatin present in the myenteric plexus and to examine some aspects of the regulatory mechanisms underlying somatostatin release and somatostatin-induced release of acetylcholine from this tissue. We observed the following: (1) Somatostatin-like immunoreactivity (SLI) is present in the myenteric plexus of the guinea pig ileum with somatostatin-14 being the predominant molecular form. (2) Somatostatin-like immunoreactivity is released from isolated myenteric ganglia after stimulation with veratridine or the ganglionic agonist dimethylphenylpiperazinium (DMPP). (3) Calcium entry via the N-type channel appears to play a dominant role in DMPP-induced release of SLI. (4) Somatostatin regulates its own release via a pertussis toxin-sensitive mechanism. (5) Under basal conditions somatostatin-14 stimulates release of acetylcholine in a concentration-dependent manner. (6) Calcium entry via L-type channels is associated with the release of acetylcholine evoked by somatostatin-14.

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