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PubMed1994

Localization of cholecystokinin A and cholecystokinin B/gastrin receptors in the canine upper gastrointestinal tract.

BACKGROUND/AIMS: Cholecystokinin (CCK) is a neuropeptide that exerts numerous effects in the gut. To determine the sites of action of CCK, the distribution and properties of CCK receptor subtypes were studied. METHODS: CCK receptors were localized by autoradiographic analysis of 125I-CCK binding to frozen sections of the canine upper gastrointestinal tract. RESULTS: In the cardiac and fundic stomach, CCK-B/gastrin receptors were found in the mucosa and in a subpopulation of neuronal elements in the circular muscle. The antrum expressed CCK-B/gastrin receptors in a few neurons in the circular muscle and in the entire myenteric plexus; no receptors were observed in the antral mucosa or esophagus. The duodenum showed a high concentration of CCK-B/gastrin receptors in the myenteric plexus. The cardiac and fundic basal mucosae expressed CCK-A receptors. Two nonpeptide CCK receptor antagonists were unable to differentiate between the receptor subtypes. CONCLUSIONS: The differential expression of CCK receptor subtypes in the gastric mucosa provides a morphological basis for the separate regulatory roles of CCK and gastrin in gastric function. CCK-B/gastrin receptor expression in a subset of neurons in gastric circular muscle suggests a novel site of action for CCK and/or gastrin.

Animals↗

PubMed1993

Visceral neuropathy in slow transit constipation: an immunohistochemical investigation with monoclonal antibodies against neurofilament.

PURPOSE: The aim of this study was to investigate neuropathologic changes in the colonic wall of patients with slow transit constipation using monoclonal antibodies raised against neurofilament. METHODS: In a prospective study, 227 patients with severe, long-standing constipation and intractable defection disorders were analyzed according to a standard protocol. Slow transit constipation was diagnosed in 65 patients (29 percent). Forty-three patients (7 men and 36 women; mean age, 46 years; range, 16-76 years) underwent a partial (n = 20) or subtotal (n = 23) colectomy. In 39 patients (5 with megacolon and 34 with normal-sized colon) the cause of their constipation remained unexplained (idiopathic slow transit constipation). All resected colon specimens were investigated with the monoclonal antineurofilament antibody NF2F11 and compared with those of 20 control patients. RESULTS: In all controls the myenteric plexus revealed a moderate and diffuse axonal staining. In 29 of 39 patients with "idiopathic" slow transit constipation, the apparently normal axon bundles in the myenteric plexus stained markedly less than normal or failed to stain at all with the monoclonal antibody. In 17 patients this reduced or absent neurofilament expression was found along the entire length of the colon, whereas in 12 patients only a portion of the colon was affected. CONCLUSION: These findings indicate that a visceral neuropathy seems to be present in the majority of patients with severe, so-called idiopathic slow transit constipation.

Adolescent↗

PubMed1999

Morphometry and acetylcholinesterase activity of the myenteric neurons of the mouse colon in the chronic phase of experimental Trypanosoma cruzi infection.

The myenteric plexus of the proximal colon, midcolon, and distal colon was studied in mice chronically infected with the Y strain of Trypanosoma cruzi by means of histochemical methods for NADH-diaphorase and acetylcholinesterase (AChE) on whole mount preparations. Ganglia of infected mice displayed an irregular distribution, with neurons severely altered in form and were found side by side with slightly degenerated or morphologically normal ones. Significant reductions of at least 36% in the numbers of neurons were recorded in all regions of the colons of infected animals, especially in the distal colon where the neuron number decreased by more than 44%. Measurements of neuron size suggest that the neuronal destruction caused by T. cruzi affected the medium and large neurons. The small neurons apparently were not affected by the infection. The histochemical demonstration of AChE by the direct coloring copper ferrocyanide method showed that in the control animals, most of the neurons of the plexus displayed AChE activity in the cytoplasm although the neurons showed different reaction intensities. The AChE activity was also present, but at a lower intensity, in the myenteric plexus of the colons of infected animals. These results suggest that the T. cruzi infection affects some categories of neurons and implies that some particular enteric neurotransmitter systems could be affected and the potency of their action upon intestinal function consequently reduced.

Acetylcholinesterase↗

PubMed1983

Hunter' syndrome. Ultrastructural features in young children.

Ultrastructural abnormalities in two stepbrothers with Hunter's syndrome, ages 1 and 4 years, were found in cortical neurons, neurons of the myenteric plexus, and skin. Inclusions containing little or no electron-dense material were noted in most tissues, and lamellar figures were restricted to cortical neurons and neurons of the myenteric plexus. These changes correlate with those described in tissues obtained at post mortem.

Cerebral Cortex↗

PubMed1974

A nervous mechanism for descending inhibition in guinea-pig small intestine.

1. Intracellular recordings were made from neurones in the myenteric plexus of guinea-pig small intestine under conditions in which these neurones received synaptic input from an adjacent segment of intestine.2. Most long synaptic pathways in the myenteric plexus were found to lead in an anal direction.3. Such pathways could be excited by either distension or transmural electrical stimulation of the intestinal segment.4. Similar stimuli evoked inhibitory junction potentials in the circular muscle layer but only on the anal side of the stimulated region of intestine.5. The results are discussed in relation to the concept of descending inhibition (Bayliss & Starling, 1899).

Action Potentials↗

PubMed2000

Projections and neurochemical coding of motor neurones to the circular and longitudinal muscle of the guinea pig gastric corpus.

The present study identified projection and neurochemical coding patterns of intrinsic circular (CMN) and longitudinal muscle motor neurones (LMN) in the guinea pig stomach by using the retrograde tracer DiI (1,1'-didodecyl-3,3,3',3'-tetramethylindocarbocya-nine perchlorate) in combination with the immunohistochemical demonstration of choline acetyltransferase (ChAT), enkephalin (ENK), neuropeptide Y (NPY), nitric oxide synthase (NOS) and substance P (SP). Populations of LMN and CMN had similar neurochemical coding and a clear polarity of projection. Taking all DiI-labeled cell bodies as 100%, ascending pathways exhibited the coding ChAT/- (CMN:14.7%/LMN: 18.3%), ChAT/ENK (15.7%/10.1%), ChAT/SP/+/-ENK (19.2%/16.4%), or ChAT/NPY (4.4%/7.6%); descending pathways had the coding NOS/- (13.8%/16.9%), NOS/NPY (9.9%/17%), NOS/ENK (4.4%/1.2%) or NOS/NPY/ENK (13.0%/5.5%). The relative contributions of these populations were not different between CMN and LMN. However, target-specific projection patterns were revealed: most LMN (82%) had longitudinal whereas most CMN (58%) had circumferential projection preferences. The results indicate that gastric circular and longitudinal muscle layers are innervated by ascending excitatory and descending inhibitory pathways in the myenteric plexus. The projection patterns of CMN and LMN were different and followed the orientation of the muscle layers. It is suggested that the specific muscle motor pathways in the gastric myenteric plexus coordinate the reflex-mediated phasic and tonic activity of gastric muscle layers.

Animals↗

PubMed1998

Identification of neurons that express stem cell factor in the mouse small intestine.

BACKGROUND & AIMS: Enteric neurons in the murine intestine express stem cell factor (SCF), which may provide an important signal in the development of the interstitial cells of Cajal (ICC). Our aim was to identify the subpopulation(s) of myenteric neurons that express SCF. METHODS: Myenteric plexus preparations from postnatal SCF-lacZ mice were processed for beta-galactosidase histochemistry followed by immunohistochemistry. RESULTS: Approximately 60% of the nitric oxide synthase-immunoreactive neurons, which projected to myenteric ganglia and to circular muscle, expressed SCF, and more than 80% of the calbindin-immunoreactive neurons, which projected exclusively to myenteric ganglia, expressed SCF. A small subpopulation of calretinin-immunoreactive neurons expressed SCF transiently. Many of the remainder of SCF-expressing neurons were choline acetyltransferase immunoreactive, but their projections are unknown. CONCLUSIONS: SCF-expressing neurons that project within the myenteric plexus may be an important source of SCF for the development of Kit-expressing ICC at this level. The only possible neuronal source of SCF for the ICC of the deep muscular plexus is a subpopulation of nitric oxide synthase-immunoreactive neurons.

Animals↗

PubMed2000

Shapes and projections of tertiary plexus neurons of the guinea-pig small intestine.

The axons of neurons that innervate the longitudinal muscle of the small intestine in small mammals such as rabbit, rat, guinea pig and mouse form a network, the tertiary plexus, against the inner surface of the muscle. In general, because of their substantial overlap, it has not been possible to follow the ramifications of individual axons in the tertiary plexus. In the present work, the longitudinal muscle motor neurons were filled with marker dyes through an intracellular microelectrode, and their morphologies and projections were examined in whole-mount preparations of longitudinal muscle and myenteric plexus. Most neurons that were examined were in the small intestine (ileum and duodenum), but a few were examined in the distal colon. Neurons in all regions had similar morphologies and projections. The cell bodies were amongst the smallest in myenteric ganglia, with major and minor axes of 14 microns and 25 microns (mean, n = 40) in the plane of the myenteric plexus. Each neuron had a single axon that branched extensively in the tertiary plexus, most had multiple lamellar dendrites and a few had filamentous dendrites or a mixture of filamentous and lamellar dendrites. The mean area of muscle covered by an axon and its branches extended 1.6 mm orally to anally and 1.7 mm circumferentially. The area covered was 2.8 +/- 1.9 mm2 (mean +/- SD, n = 23). From the density of occurrence of cell bodies, it can be calculated that each point in the longitudinal muscle is innervated by the processes of about 100 motor neurons and is influenced by electrotonic conduction of signals through the muscle by about 300 motor neurons.

Animals↗

PubMed1986

Ontogeny of substance P in the digestive tract, spinal cord and hypothalamus of the human fetus.

The time of appearance and tissue concentrations of substance P-like immunoreactivity (SP-LI) were studied in 53 human fetuses aged 8-21 weeks. Detectable amounts were present at 8 weeks of gestation in available fragments of spinal cord and intestine. Thereafter, the tissue concentrations were highest in spinal cord, intermediate in hypothalamus and lowest in digestive tract. Except for a significant increase in the intestinal wall, the concentrations did not vary from the 8-14 to the 15-21 week period. At chromatography, SP-LI in extracts of spinal cord and intestine was essentially eluted in the volume of the synthetic undecapeptide. Using the indirect immunofluorescence technique, the localization of SP-LI positive structures in the digestive tract was studied in 5 fetuses aged 12-18 weeks. Scarce cell bodies were observed in the myenteric plexus. Nerve fibers were recognized in the muscular layer, in the myenteric plexus and in connective tissue of pancreas. The present results demonstrate the early appearance of SP-LI positive structures both in central nervous system and in the enteric nervous system in the human fetus. In the age range tested, SP-LI concentrations were noticeably higher in spinal cord and hypothalamus than in the digestive tract.

Digestive System↗

PubMedDate not supplied

[Familial syndrome combining short small intestine, intestinal malrotation, pyloric hypertrophy and brain malformation. 3 anatomoclinical case reports].

Anatomoclinical study of 3 cases of an exceptional malformative condition characterized by: --extreme shortness of the small intestine, --mesenterium commune, --hypertrophic pylorus, --malformation of the central nervous system (heterotopia, absence of operculum temporale). Clinically this malformative condition is characterized by failure and inertia of the intestinal peristalsis producing at intervals of 10-15 days episodes of subocclusion, the repetition of which causes death. The syndrome is familial and seems to be of autosomal recessive inheritance. The absence of mechanical obstruction, the repeated failure of colostomy and ileostomy, the normal aspect of the myenteric plexuses verified by cytoenzymatic and silver stains allow to individualize this anatomoclinical syndrome and to rule out the hypothesis of Hirschsprung's disease, Chagas' disease, idiopathic megacolon or hypoplasia of the myenteric plexuses. The association of cerebral malformations leads to consider the responsibility of a lack of synthesis of a same specific intermediate factor which is up to now poorly determined, implicated in the neuronal migration and neuromuscular transmission.

Abnormalities, Multiple↗

PubMed1987

Inhibitory effect of ionized free intracellular calcium enhanced by ruthenium red and m-chloro-carbonylcyanide phenyl hydrazon on the evoked release of acetylcholine.

In order to understand the relationship between the free ionized calcium concentration in the axon terminals and the transmitter release we have investigated the effect of ruthenium red (RuR) and m-chloro-carbonylcyanide phenyl hydrazon (CCCP), mitochondrial uncoupler agents on the liberation of acetylcholine from myenteric plexus of guinea-pig ileum. Both compounds are able to enhance intracellular free Ca2+. In the presence of RuR and CCCP the spontaneous release of radioactivity from isolated myenteric-plexus preparation, previously loaded with (methyl-3H)-choline chloride was significantly enhanced while that evoked by electrical stimulation was decreased. Atropine did not affect the electrically evoked release in the presence of CCCP, indicating that in the effect of CCCP the presynaptic muscarinic receptors mediated negative feedback modulation does not play any role. Our findings are consistent with the hypothesis that the enhanced level of intracellular free Ca2+ enhances the spontaneous while depresses the electrically evoked release of transmitter.

Acetylcholine↗

PubMed1981

Intracellular proteins that bind serotonin in neurons, paraneurons and platelets.

1. Properties of serotonin binding proteins (SBP) extracted from neuroectodermal derivatives (brain, myenteric plexus, thyroid parafollicular cells) were found to differ from serotonin binding proteins extracted from cells of mesodermal (platelets) or entodermal (intestinal mucosa) origin. 2. Serotonin binding proteins extracted from brain, myenteric plexus, and thyroid parafollicular cells all had similar properties. 3. Binding of tritiated serotonin to serotonin binding protein is inhibited by a drug that interferes with intracellular storage of serotonin (reserpine) or by exposing the protein to extracellular salt concentrations (Krebs solution). 4. It is proposed that serotonin binding protein is a neuron-specific storage protein for serotonin that serves to decrease intravesicular osmotic pressure, and that serotonin dissociates from a complex with the protein when the lumen of synaptic vesicles is exposed to extracellular fluid at the time of exocytosis.

Animals↗

PubMed2000

CCK-A receptor activation induces fos expression in myenteric neurons of rat small intestine.

Cholecystokinin (CCK), a hormone secreted from endocrine cells of the small intestine, participates in the control of motility and secretion in the gastrointestinal tract, and in the control of food intake. At least some of the effects of CCK on intestinal function appear to be mediated via activation of intrinsic neurons in the myenteric plexus. However, the distribution of CCK-responsive enteric neurons within the rat small intestine is not known. Neither has the role of CCK-A receptors in the activation of rat myenteric neurons been investigated. Therefore, to determine the distribution of CCK-responsive neurons in the small intestinal myenteric plexus we utilized immunohistochemical detection of Fos, the protein product of the immediate early gene c-fos, to identify neurons that were activated by exogenous CCK. We also monitored Fos expression in the dorsal hindbrain, and examined CCK-induced Fos expression in the presence or absence of a receptor antagonist for the type-A CCK receptor. We found that CCK significantly increased Fos expression in the hindbrain and in myenteric neurons of the duodenum and jejunum, but not the ileum. Neuronal Fos responsiveness in both brain and myenteric neurons was mediated by CCK-A receptors, as CCK-induced Fos expression was eliminated in rats pretreated with a CCK-A receptor antagonist. We conclude that CCK activates small intestinal myenteric neurons, via CCK-A receptors. Activation of these intrinsic intestinal neurons may participate in reflexes and behaviors that are mediated by CCK.

Animals↗

PubMed1987

Antibodies to fragments of provasoactive intestinal peptide reveal subpopulations of vasoactive intestinal peptide containing neurons in the rat gut.

The cellular origin of peptides derived from preprovasoactive intestinal peptide has been studied in rat stomach and ileum. Antisera specific for the C-terminal regions of the N-terminal flanking peptide (preprovasoactive intestinal peptide 22-80), bridging peptide (preprovasoactive intestinal peptide 111-124), C-terminal flanking peptide (preprovasoactive intestinal peptide 156-170) and vasoactive intestinal peptide were used in immunohistochemical studies on sections and whole mounts. All four antisera stained nerve fibres and cell bodies in the stomach and intestine. However, there were distinct differences in the pattern of colocalization of peptides derived from provasoactive intestinal peptide. In the sub-mucous plexus of the ileum virtually 100% of neurons reacting with vasoactive intestinal peptide antibodies also reacted with antibodies to the other three peptides. In contrast, in the stomach, while all vasoactive intestinal peptide-immunoreactive neurons of the myenteric plexus contained C-terminal flanking peptide- and bridging peptide-like immunoreactivity, only 50% of these cells reacted with the antiserum to N-terminal flanking peptide. The data indicate that in a population of neurons in the myenteric plexus of the rat stomach, preprovasoactive intestinal peptide is processed in such a way that the antigenic determinant of the N-terminal flanking peptide is not produced. In a second population of enteric neurons in the stomach, and in the intestine, it appears that processing of preprovasoactive intestinal peptide results in the production of peptides reacting with antibodies to vasoactive intestinal peptide, the flanking and bridging peptides.

Animals↗

PubMed1990

Myoelectric activity of small intestine after chemical ablation of myenteric neurons.

Ablation of the myenteric plexus was performed by serosal application of 0.062% benzalkonium chloride (BAC) in the duodenum, proximal and distal jejunum, and ileum. The thickness of muscle layers and the number and sizes of ganglia and neurons of the myenteric plexus were evaluated before and 21-28 days after treatment. Electrodes were implanted on the treated segments and on segments orad and aborad to the treated segment. The electromyogram of each segment was recorded daily for periods of 2-3 h. The number of myenteric neurons in the BAC-treated segment was decreased significantly by 85 to 98% relative to segments removed before BAC application. Significantly, thickening of longitudinal plus circular muscle layers amounted to 113% in the duodenum and 261% in the ileum in the treated segment. No changes were observed in electrical slow-wave frequency in treated segments. Spike activity (percentage of slow waves with spikes) increased in the BAC-treated segment by 92% compared with recording sites orad and aborad to the treated segment and to the small intestine in untreated control animals. We interpreted the increase in spike activity in treated segments to reflect the loss of inhibitory neuronal influence. The hyperplasia and hypertrophy of the longitudinal and circular muscle coat could have resulted from a direct influence of the altered innervation or from work-induced hypertrophy in the treated segment secondary to uncoordinated hyperactivity of the disinhibited musculature.

Action Potentials↗

PubMed1984

Origin of sensation in the esophagus.

The sensory innervation of the esophagus is important both to physicians, for whom esophageal sensation can cause clinical confusion, and to physiologists, who wish to understand the regulation of esophageal motion. Sensory mechanisms in the gut in general are not well understood. Mechanoreceptive reflexes and their pathways, both parasympathetic and sympathetic, have been studied in the esophagus, and thermoreceptive reflex pathways that are parasympathetic have recently been described. The terminal sensory innervation of the esophagus contains several structures that may be receptors to such stimuli. Esophageal striated muscle contains muscle spindles like those of somatic muscle. Within the myenteric plexus, the bodies of certain ganglion cells themselves may be mechanoreceptive. Also, complex subcapsular laminar arborizations that arise from cells of the nodose ganglion have been described in ganglia of the esophageal myenteric plexus. Similar laminar arborizations have been found on vessels of the submucosa in the midesophagus. In the esophageal mucosa, the terminal innervation ends in structures of diverse form located both superficially and deep in the squamous epithelium. Thus, a variety of specific neural structures that seem to represent the terminals of sensory nerves exist in the esophagus and may serve the mechanoreceptive and thermoreceptive reflexes that modify esophageal motility.

Animals↗

PubMed1986

Localization of Met-enkephalin-Arg6-Gly7-Leu8 immunoreactivity in rat duodenum.

The distribution of Met-enkephalin-Arg6-Gly7-Leu8 (Met-ENK-Arg6-Gly7-Leu8) in the rat duodenum was determined using specific antibodies against Met-ENK-Arg6-Gly7-Leu8 and the immunofluorescence microscope technique. Met-ENK-Arg6-Gly7-Leu8 immunoreactive perikarya have been detected in the myenteric plexus. These neuronal cell bodies were large in diameter and round in shape. Met-ENK-Arg6-Gly7-Leu8 immunostained nerve fibres were noted in both the circular muscle layer and, more abundantly, in interconnecting myenteric plexus nerve fibre bundles. These findings might indicate that Met-ENK-Arg6-Gly7-Leu8 has important physiological roles as neurotransmitter and/or neuromodulator in the human and mammalian gastrointestinal tract.

Animals↗

PubMed1987

Selective damage of intrinsic calcitonin gene-related peptide-like immunoreactive enteric nerve fibers in streptozotocin-induced diabetic rats.

The distribution of calcitonin gene-related peptidelike immunoreactive (CGRP-LI) nerve fibers in the myenteric plexus of ileum and proximal colon of rats 8 wk after induction of diabetes with streptozotocin was studied using immunohistochemical techniques. A marked decrease in CGRP-LI nerve fibers mainly around the ganglion cells of the myenteric plexus of both ileum and proximal colon was observed in diabetic rats. The sparsely located immunoreactive nerve cell bodies in the control rats were absent in the diabetic preparations. There were, however, intensely stained CGRP-LI varicose nerve fibers that ran through the internodal strands and over the myenteric ganglia of the diabetic intestines. These findings indicate the presence of CGRP-LI nerve fibers of dual origin in the intestinal wall. The absence of positive cell bodies and diminished CGRP-LI nerve fibers around the ganglion cells in the diabetic tissues suggest that the state of diabetes selectively affects CGRP-LI nerve fibers of intrinsic rather than extrinsic origin. Furthermore, the absence of change in substance P-like immunoreactivity in the enteric system of rats with streptozotocin-induced diabetes of the same duration suggests that calcitonin gene-related peptide and substance P are contained in different populations of intrinsic nerve fibers in the gastrointestinal tract of the rat.

Animals↗