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PubMed1980

Evidence for vagal enkephalinergic neural control of the feline pylorus and stomach.

The atropine- and guanethidine-resistant contraction of the cat pyloric sphincter induced by efferent stimulation of the cervical vagi, was studied with a new method for measuring transpyloric flow. The pyloric contraction was blocked in a dose-dependent manner by the opiate antagonist naloxone infused intraarterially to the pyloric region. Local intraarterial injection of morphine or enkephalinamide elicited a pyloric and gastric contraction. Leu- and met-enkephalin intraarterially elicited a pyloric contraction and a gastric relaxation. These effects could be prevented or reversed by naloxone. Immunohistochemical studies revealed a particularly rich enkephalinergic innervation of the pylorus with dense networks of varicose nerve fibers with enkephalin-like immunoreactivity both in the circular smooth muscle layer and in the myenteric plexus. Furthermore, many cell bodies of the myenteric plexus with enkephalin-like material were demonstrated. The corpus-antrum was sparsely innervated by enkephalin-like nerves to the circular muscle layer and only few immunoreactive cell bodies were observed in the myenteric plexus. These results together suggest a vagal control of the feline pylorus and stomach mediated via enkephalinergic neurons.

Animals↗

PubMed1989

[Effect of enteric nervous system on anti-peristaltic discharge].

The mechanism of the occurrence of anti-peristaltic discharge originated in the stomach distal to the transection followed by end-to-end anastomosis has not been elucidated. The purpose of this study is to investigate the effect of the enteric nervous system on the anti-peristaltic discharge in the canine stomach distal to the transection by using sodium channel blocking agent TTX and ganglion blocking agent C6 together with local anesthetic lidocaine electromyographycally. Following results were obtained. 1. The retardation of propagation velocity of normo-peristaltic discharge and the decrease of frequency of anti-peristaltic discharge were noted both at TTX 10 micrograms/kg iv. and TTX 10 micrograms/kg iv. together with mucosal anesthetization by lidocaine. And no significant difference was recognized between them. 2. The retardation of propagation velocity of normo-peristaltic discharge and the decrease of frequency of anti-peristaltic discharge were noted at C6 10 mg/kg iv. together with mucosal anesthetization by lidocaine. While the decrease of frequency of anti-peristaltic discharge was only noted at C6 10 mg/kg iv. Conclusively, it was suggested that the nervous pathway which transmits some excitive information from mucosa to the myenteric plexus exists and that the myenteric plexus has a important role on the occurrence of anti-peristaltic discharge.

Action Potentials↗

PubMed2004

Role of galanin receptor 1 in peristaltic activity in the guinea pig ileum.

Galanin effects are mediated by distinct receptors, galanin receptor 1 (GAL-R1), GAL-R2 and GAL-R3. Here, we analyzed 1) the role of GAL-R1 in cholinergic transmission and peristalsis in the guinea-pig ileum using longitudinal muscle-myenteric plexus preparations and intact segments of the ileum in organ bath, and 2) the distribution of GAL-R1 immunoreactivity in the myenteric plexus with immunohistochemistry and confocal microscopy. Galanin inhibited electrically stimulated contractions of longitudinal muscle-myenteric plexus preparations with a biphasic curve. Desensitization with 1 microM galanin suppressed the high potency phase of the curve, whereas the GAL-R1 antagonist, RWJ-57408 (1 microM), inhibited the low potency phase. Galanin (3 microM) reduced the longitudinal muscle contraction and the peak pressure, and decreased the compliance of the circular muscle. All these effects were antagonized by RWJ-57408 (1 or 10 microM). RWJ-57408 (10 microM) per se did not affect peristalsis parameters in normal conditions, nor when peristalsis efficiency was reduced by partial nicotinic transmission blockade with hexamethonium. In the myenteric plexus, GAL-R1 immunoreactivity was localized to neurons and to fibers projecting within the plexus and to the muscle. GAL-R1 was expressed mostly by cholinergic neurons and by some neurons containing vasoactive intestinal polypeptide or nitric oxide synthase. This study indicates that galanin inhibits cholinergic transmission to the longitudinal muscle via two separate receptors; GAL-R1 mediates the low potency phase. The reduced peristalsis efficiency could be explained by inhibition of the cholinergic drive, whereas the decreased compliance is probably due to inhibition of descending neurons and/or to the activation of an excitatory muscular receptor. Endogenous galanin does not appear to affect neuronal pathways subserving peristalsis in physiologic conditions via GAL-R1.

Acetylcholine↗

PubMed1986

Immunohistochemical demonstration of GABAergic neurons in the enteric nervous system.

Application of a highly specific antiserum against GABA to whole-mount preparations of the guinea pig and rat myenteric plexus resulted in discrete and unambiguous immunolabeling of a subpopulation of myenteric neuronal cell bodies and fibers. The anti-GABA antiserum, which was raised against GABA conjugated by glutaraldehyde to BSA, was applied to glutaraldehyde-fixed whole mounts and subsequently visualized using the peroxidase-antiperoxidase method. In the guinea pig ileum and colon, immunoreactive varicose nerve fibers and scattered nerve cell bodies were found within the myenteric plexus. Immunostained fibers were also seen in the tertiary plexus and in the circular muscle, running parallel to the muscle bundles. GABA immunoreactivity in these intramuscular nerves was most pronounced in the colon. In the rat, immunoreactive fibers were prominent throughout the myenteric plexus. They formed dense networks within the myenteric ganglia, which also contained immunopositive nerve cell bodies, and ran between them in the interconnecting nerves. Some immunoreactive nerve fibers were seen in the circular muscle. Control experiments using non-immune sera or adsorbed anti-GABA antiserum showed no staining. These results add a definitive support to our previous suggestion that GABA serves as an autonomic neurotransmitter in vertebrates. In addition to the present immunohistochemical evidence, this hypothesis is supported by biochemical, autoradiographic, transmitter release, electrophysiological, and pharmacological studies on the enteric nervous system of several species. It is now important to determine the functional role of GABAergic neurons within the complex neuronal circuitry that controls gut functions.

Animals↗

PubMed1993

Grafting in acute spinal cord injury: morphological and immunological aspects of transplanted adult rat enteric ganglia.

We have studied allogeneic transplants of adult rat enteric ganglia in order to evaluate their use as donor tissue for eventual autografts in rodent spinal cord injury models. Female Sprague-Dawley rats of similar weights served either as transplant donors or as recipients. A glass micropipette of 0.8 mm diameter was used to create a local penetrating injury of the lower thoracic spinal cord and the transplant material was pressure injected through the pipette within the neural parenchyma. Ganglia of the myenteric plexus adhering to the stratum longitudinal muscularis were dissected from portions of the jejunum and ileum. Following partial enzymatic digestion and mechanical disruption of the myenteric plexus and muscle tissue (labeled with adherent rhodamine conjugated microbeads), reaggregates of myenteric plexus and muscle were suspended in growth medium and cultured in vitro for one to two days prior to transplantation. Transplants were examined at three, four, six, and eight weeks after surgery. Some of the donor tissue was grown in vitro, in order to determine its cellular composition. These cultured explants were fixed after 10 days, and like myenteric plexus and muscle grafts, were stained histochemically for acetylcholinesterase and observed by fluorescence and light microscopy. At the earlier post-transplantation periods, grafts contained several clusters of enteric ganglion cells that were positive for acetylcholinesterase and exhibited ultrastructural features characteristic of the enteric nervous system. They had well-defined boundaries. Reactive astrocytes and their processes remained located within the host spinal cord adjacent to the boundary region of the grafts. Likewise, macrophages were located in areas abutting the graft. Newly formed vasculature penetrated the graft interior and appeared to be continuous with the host vessels. Grafts grown for at least eight weeks were characterized by interdigitating boundaries. Finger-like protrusions of graft tissue containing fibroblasts and collagen intermixed with adjacent gray and white matter of the host cord. Such transplants also had reactive astrocytes and ED1-positive macrophages. At this later stage, several groups of ganglion cells were identified that were intensely acetylcholinesterase-positive; however, only two of four grafts were recovered, whereas two of the transplants degenerated. We postulate that degeneration of allogeneic grafts may occur as a result of ongoing immune responses of the host which could be prevented by use of autogeneic enteric ganglia. Our studies show that fully differentiated enteric ganglia can survive transplantation to acutely injured spinal cord of adult rats.

Acetylcholinesterase↗

PubMed2004

Cholinergic, nitrergic and peptidergic (Substance P- and CGRP-utilizing) innervation of the horse intestine. A histochemical and immunohistochemical study.

The small and large intestine of adult horses were histochemically and immunohistochemically investigated in order to evidence components of the intramural nervous system. The general structural organization of the intramural nervous system was examined by using Nissl-thionin staining as well as the anti-neurofilament 200 (NF200) immunoreaction, which demonstrated the presence of neurons in the submucous as well as myenteric plexuses. The additional presence of subserosal ganglia was shown in the large intestine. Acetylcholinesterase (AChEase) activity was observed in both the submucous and myenteric plexuses. Localization of acetylcholine-utilizing neurons was also evidenced by immunohistochemical reactions for choline acetyltransferase (ChAT) and vesicular acetylcholine transporter (VAChT). With both histochemistry and immunohistochemistry possible cholinergic nerve fibres were detected in the inner musculature. The two possible cholinergic co-mediators Calcitonin Gene-Related Peptide (CGRP) and Substance P (SP) have been investigated by an immunohistochemical approach. CGRP immunoreactivity was detected in roundish nerve cell bodies as well as in nerve fibres of the submucous plexus, whereas SP immunoreactivity was evidenced in nerve fibres of the tunica mucosa, in nerve cell bodies and fibres of the submucous plexus and in nerve fibres of the myenteric plexus. NADPH-diaphorase reactivity, which is linked to the synthesis and release of nitric oxide, was detected in nerve cell bodies and nerve fibres of both the submucous and myenteric plexuses as well as in a subserosal localization of the large intestine. The nitrergic components were confirmed by the anti-NOS (nitric oxide synthase) immunoreaction. Results are compared with those of other mammals and related to the complex intestinal horse physiology and pathophysiology.

Animals↗

PubMed1992

Antagonists of nitric oxide synthesis inhibit nerve-mediated relaxations of longitudinal muscle in guinea pig ileum.

Enteric inhibitory nerves release nonadrenergic, noncholinergic (NANC) transmitters onto the muscle layers of guinea pig ileum. Nitric oxide (NO), released from endothelial cells, relaxes vascular smooth muscle and NO may also be a chemical messenger released from neurons. The present study investigated the possibility that NO is a NANC transmitter in guinea pig ileum longitudinal muscle myenteric plexus. Segments of longitudinal muscle myenteric plexus were maintained in scopolamine-containing (1 microM) Krebs' solution. Histamine (1 microM) was used to induce tone, and NANC relaxations were produced by trains of transmural electrical stimuli. NANC responses consisted of a fast relaxation (approximately 1 s duration) followed either by a slow relaxation or a slow contraction (approximately 4 s duration). The NO-synthase inhibitors, NG-monomethyl-L-arginine, NG-nitro-L-arginine and NG-nitro-L-arginine methyl ester, inhibited peak (fast) neurogenic relaxations by a maximum of 62 +/- 6%, 91 +/- 3% and 50 +/- 3%, respectively. NO-synthase inhibitors either completely blocked the slow relaxation revealing a late contraction or increased the amplitude of late contractions. The actions of NG-monomethyl-L-arginine were partially reversed by L-arginine (1 mM) while the actions of NG-nitro-L-arginine methyl ester and NG-nitro-L-arginine were not consistently reversed by L-arginine. L-Arginine itself did not alter neurogenic responses. NG-monomethyl-D-arginine (10-300 microM) did not affect NANC relaxations or contractions. Hemoglobin (10 microM) inhibited peak NANC relaxations by 45 +/- 4% and increased the amplitude of late contractions without affecting papaverine-induced relaxations. Sodium nitroprusside and 8-bromo-cyclic guanosine monophosphate mimicked NANC relaxations.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗

PubMed1989

Shapes and projections of neurons with immunoreactivity for gamma-aminobutyric acid in the guinea-pig small intestine.

The distribution of nerve cell bodies and fibres with immunoreactivity for gamma-aminobutyric acid (GABA) has been studied in the guinea-pig small intestine. Cell bodies were common in myenteric ganglia but were extremely rare in the submucosa. Reactive fibres were numerous in the tertiary component of the myenteric plexus and in the circular muscle but they were rare in both myenteric and submucous ganglia. Reactive nerve fibres were absent from the mucosa. This distribution conforms to previous descriptions. Exposure to exogenous GABA, in vitro, was used to supplement endogenous stores of GABA. The morphology of cell bodies was better defined after this treatment. Nearly all cell bodies had type-I morphology, i.e., the cells had numerous short lamellar dendrites and one axon. Most axons ran anally. Some could be traced to the tertiary component of the myenteric plexus, others to the circular muscle. Removal of the myenteric plexus from a short length of intestine caused a loss of nerve fibres from the circular muscle beneath the site of operation and a decrease in fibre density in the circular muscle that extended anally from the lesion for about 1 mm. The nerve lesions caused no significant changes in the tertiary plexus. It is concluded that GABA is contained in motor neurons supplying the longitudinal and circular muscle, and that the neurons supplying the circular muscle may be inhibitory.

Animals↗

PubMed1996

Enteric neuropeptides in streptozotocin-diabetic rats; effects of insulin and aldose reductase inhibition.

The aim of the present study was to determine whether diabetes-induced changes in the distribution of enteric neuropeptides, could be prevented in 12-week streptozotocin-diabetic rats, by rigorous control of glycaemia, using daily adminstration of insulin, or an aldose reductase inhibitor (ponalrestat). The pattern of distribution of nerve fibres and cell bodies, containing immunoreactive vasoactive intestinal polypeptide (VIP), galanin (GAL), calcitonin gene-related peptide (CGRP) and substance P was examined in the myenteric plexus of ileum from control, untreated diabetic, insulin-treated diabetic and aldose reductase inhibitor-treated diabetic rats. The increase in VIP- and GAL-like immunoreactivity, seen in the myenteric plexus of untreated diabetic rat ileum, was not present in the myenteric plexus of ileum from insulin- and aldose reductase inhibitor-treated diabetic rats. With CGRP-like immunoreactive fibres, there was a clear decrease in the ileum of untreated diabetic rats. This was prevented by insulin treatment, but aldose reductase inhibitor treatment had no effect. No alterations in substance P-like immunoreactivity were seen in the myenteric plexus of ileum from any of the groups investigated. Generally, the similarity of effect of ponalrestat and insulin on VIP and galanin expression in this study supports a primary effect of insulin via glycaemic control. The dissimilarity of the effect of the two treatments on CGRP expression may imply a neurotrophic effect of insulin, although there are certainly consequences of hyperglycaemia other than exaggerated flux through the polyol pathway.

Aldehyde Reductase↗

PubMed1985

Dynorphin-A (1-8) is contained within perikarya, nerve fibres and nerve terminals of rat duodenum.

By the use of well-characterized antibodies against porcine dynorphin-A(1-8), an endogenous opioid peptide, and the use of a modified immunofluorescence microscopic technique, dynorphin-A(1-8) stained perikarya, nerve fibres, and nerve terminals were visualized in the rat duodenum. Dynorphin-A(1-8) immunoreactive perikarya were revealed with certainty only in the myenteric plexus, while dynorphinergic nerve fibres could bee seen in the myenteric plexus and circular muscle layer, but not in the longitudinal muscle layer and submucous plexus. Dynorphin-A(1-8) immunofluorescent nerve endings were in close contacts with submucosal blood vessels, probably arterioles, and Brunner's gland cells. These findings suggest that the opioid peptide dynorphin-A(1-8) might be synthetized within myenteric plexus perikarya of the rat duodenum and that it might modulate the peristaltic activity, intestinal blood pressure, and production of mucopeptides synthetized within Brunner's gland cells.

Animals↗

PubMed1999

Urocortin mRNA is expressed in the enteric nervous system of the rat.

The expression of the urocortin gene in the gastrointestinal tract was investigated using reverse transcription polymerase chain reaction (RT-PCR) and in situ hybridization histochemistry. PCR demonstrated the presence of urocortin mRNA in the rat brain, duodenum, small intestine, and colon. By in situ hybridization, urocortin-containing cells were exclusively localized to the submucosal plexus and myenteric plexus in the duodenum, small intestine and colon. These results suggest that urocortin may play an important role in the regulation of gastrointestinal motor function throughout the enteric nervous system.

Animals↗

PubMed1983

Rectal myenteric nerve plexus stimulation in Hirschsprung's disease and in healthy children.

The internal anal sphincter response was studied manometrically while applying electrical stimulation to the rectal mucosa. Seven patients with Hirschsprung's disease and ten healthy controls were investigated during general anaesthesia. In addition, six healthy controls were examined when awake. Internal sphincter relaxations elicited by electrical stimulation of the rectal myenteric nerve plexus were recorded in all anaesthetized controls, but in only two of the patients. The latter required a higher stimulation voltage. Rectal myenteric nerve plexus stimulation is a theoretical alternative for the diagnosis of Hirschsprung's disease. One advantage over conventional manometry is that it avoids the risk of mechanical artifacts. Further studies are necessary to evaluate whether the method can be of practical importance in neonatal diagnosis of Hirschsprung's disease.

Anesthesia↗

PubMed1997

Neurochemical coding in the small intestine of patients with Crohn's disease.

BACKGROUND: There have been conflicting results regarding the effect of Crohn's disease on the neurochemical composition of the enteric nervous system. AIMS: To examine the effect of Crohn's disease on the neurochemical composition of enteric nerve fibres and cell bodies using whole mount preparations of human ileum. METHODS: Whole wall ileum from seven normal subjects and nine patients with Crohn's disease was used to investigate the neurochemical composition of neurones and nerve fibres in the myenteric plexus, circular muscle, and serosa layer of ileum using immunohistochemical techniques. RESULTS: Increased tyrosine hydroxylase, 5-hydroxytryptamine, and neuropeptide Y immunoreactivity was exclusively seen in the myenteric plexus. There was increased neurofilament immunoreactivity in the myenteric plexus and nerve fibres of the circular muscle layer, and thick bundles of immunoreactive nerve fibres in the serosa layer. Increased vasoactive intestinal polypeptide, nitric oxide synthase, and pituitary adenylate cyclase activating peptide immunoreactivity was seen in the myenteric plexus and nerve fibres of the circular muscle layer, and aggregates of inflammatory cells in the serosa layer of the afflicted segment of Crohn's ileum. In addition, there was a chaotic display of nerve fibres containing some of the neuroactive substances with a high frequency of enlarged varicosities in the myenteric ganglia and/or nerve fibres of the circular muscle layer of Crohn's ileum. CONCLUSION: Results show quantitative as well as qualitative changes in the neurochemical composition of enteric nerve fibres and nerve cell bodies of Crohn's ileum. These changes and the presence of nitric oxide synthase and peptides immunoreactive inflammatory cells in the serosa layer suggest that nerve-immune interactions may have a significant role in the process of the inflammatory changes seen in Crohn's ileitis.

Adult↗

PubMed1991

Evidence that myenteric neurons of the gastric corpus project to both the mucosa and the external muscle: myectomy operations on the canine stomach.

The distribution of nerve cell bodies and fibres in the canine stomach was investigated using antibodies to the general neuronal marker, neuron-specific enolase. Prominent ganglia containing many reactive nerve cells were found in the myenteric plexus of the gastric corpus and antrum. Nerve cells were absent from the submucosa of the corpus and were extremely rare in the antrum. Removal of areas of longitudinal muscle and myenteric plexus from the corpus (myectomy), with 7 days allowed for axon degeneration, resulted in the loss of fibres reactive for galanin, gastrin-releasing peptide, substance P and vasoactive intestinal peptide from both the circular muscle and mucosa in the area covered by the lesion. Combined vagotomy and sympathetic denervation did not significantly affect these fibres, but did cause fibres reactive for calcitonin gene-related peptide to degenerate. It is concluded that the myenteric plexus of the gastric corpus, like the myenteric plexus of the small intestine and colon, is the source of nerve fibres innervating the circular muscle, but, in contrast to other regions of the gastrointestinal tract, myenteric ganglia, not submucous ganglia, are the major, or sole, source of the intrinsic innervation of the mucosa.

Animals↗

PubMed1978

A familial neuronal disease presenting as intestinal pseudoobstruction.

The purpose of this paper is to describe 2 siblings who had a generalized neurological disease which presented as intestinal pseudoobstruction. The siblings had 40-year histories of abdominal pain, distention, and vomiting as well as gait ataxia, small, irregular, poorly reactive pupils, dysarthria, absent deep tendon reflexes, and impaired vibratory and position senses. Compared with age-matched controls, they had inappropriate blood pressure responses to phenylephrine, the Valsalva maneuver, and upright posture, lack of sweating on warming, and pupillary denervation hypersensitivity. Radiographs revealed hyperactive, nonpropulsive contractions of a dilated esophagus and small intestine and extensive colonic diverticulosis. Esophageal manometry recorded repetitive, spontaneous, nonperistaltic waves and positive Mechyolyl tests. Postmortem examinations showed degeneration of the myenteric plexuses of the esophagus, small intestine, and colon of both patients. Myenteric plexus neurons were significantly reduced in number compared with 7 controls. About one-third of the siblings' neurons contained round, eosinophilic intranuclear inclusions, which, by histochemistry, were composed of protein by lacked RNA, DNA, carbohydrate, and fat. By electron microscopy the inclusions consisted of an irregular array of nonviral, nonmembrane-bounded filaments. Neurons and glial cells of the brain, spinal cord, dorsal root, and celiac plexus ganglia contained identical intranuclear inclusions. Intestinal smooth muscle was normal. These 2 siblings represent a unique disease in which degeneration of the myenteric plexus resulted in hyperactive but uncoordinated smooth muscle activity and the clinical syndrome of intestinal pseudoobstruction, the presenting manifestation of their neurological disease.

Brain↗

PubMed1987

Role of substance P in post-tetanic potentiation in myenteric plexus-longitudinal muscle preparations; the effect of substance P-antagonist.

A role of substance P in post-tetanic potentiation in the myenteric plexus-longitudinal muscle preparation of the guinea-pig ileum was investigated by means of substance P-antagonist, (D-Pro2, D-Trp7,9)-substance P. After the addition of substance P-antagonist (10(-7)-10(-5) mol x l-1) a dose-dependent reduction of post-tetanic potentiation of neurogenic twitches was observed. Post-tetanic potentiation was actually abolished in the presence of 10(-5) mol x l-1 substance P-antagonist. It has been shown previously by our group that post-tetanic potentiation is reduced in preparations desensitized by substance P; this, together with our present results supported the hypothesis that the release of substance P-like compounds during tetanic stimulation played a key role in the mechanism of post-tetanic potentiation.

Animals↗

PubMed1996

Sequential pattern of nerve-muscle contacts in the small intestine of developing human fetus. An ultrastructural and immunohistochemical study.

The developing enteric nervous system of the human fetus has been studied by means of electron microscopy and neuron-specific enolase immunocytochemistry between the 10th and 26th week of gestation, with special reference to the development of nerve-muscle contacts. In the 10th week of gestation the circular muscle layer is formed, followed by the appearance of a primitive myenteric plexus, and the longitudinal smooth muscle layer in the 12th week of gestation. Adherens-type junctions between the smooth muscle cells and the elements of the myenteric plexus, interdigitation of nerve and muscle processes, and also contacts without any morphological specialization are frequent until the 18th week, when the mechanical points of attachment are relocated from the circular to the longitudinal muscle layer. By this time the developing myenteric plexus becomes ensheathed by non-neuronal cells, disrupting the direct contacts between smooth muscle cells and the primary strands of the myenteric plexus. The possible functional significance of these changing nerve-muscle contacts is discussed in the present paper.

Abortion, Legal↗

PubMed1994

Abnormal distribution of nerve terminals in infantile hypertrophic pyloric stenosis.

Smooth muscle biopsy specimens obtained from nine infants with infantile hypertrophic pyloric stenosis (IHPS) and from three controls were studied immunohistochemically with respect to the distribution of nerve terminals and neurofilaments. To label nerve terminals and neurofilaments, monoclonal antibodies (MAb) 171B5 and 2F11 were used, respectively. In all specimens of the control group, nerve terminals were numerous in both the myenteric plexus and the muscle layer. There were abundant neurofilaments in the myenteric plexus and a moderate number in the muscle layer. In all specimens of the IHPS group, the density of nerve terminals and neurofilaments was reduced in the muscle layer. In the myenteric plexus, there was no such reduction. The results indicate poor neuronal innervation of the muscle layer in the pylorus of infants with IHPS. This poor innervation may be related to the pathogenesis of pyloric stenosis and hypertrophy.

Antibodies, Monoclonal↗