Intestinal Plexus Research Articles

ELECTRONIC-MICROSCOPIC CHANGES OF THE INTRAMURAL NERVOUS PLEXUS OF THE DUODENUM IN CONDITIONS OF CHRONIC STRESS

The article presents a study of ultrastructural changes of neurons of the intramural nervous system (muscular- intestinal plexus) of the duodenum under chronic stress. The experiment was performed on 60 white adult male rats. The material was taken from the proximal and distal parts of the duodenum after 14, 28, 56 days of the experiment. For electron microscopic examination, pieces of the duodenum were fi xed in 2.5% glutaraldehyde solution for 4 hours, and then fi xed in 2% osmium tetroxide solution. First, semi-thin sections were made to detect the localization of nerve cells of the musculoskeletal plexus of the duodenum, staining them in 1% methylene blue solution or 0.1% toluidine blue solution. Ultrathin sections were made on an ultramicrotome Tesla BS-490A, the material was studied on an electron microscope TEM – 125 K («Selmi», Ukraine). After 14 days of chronic stress, there is signifi cant damage to the neurons of the musculoskeletal plexus of the duodenum due to reactive and edematous processes, accompanied by the development of ultrastructural changes and the death of some neurons. After 28-56 days of the experiment, edematous, dystrophic- destructive processes in nerve cells are further observed, but in some of them there are a number of compensatory- adaptive and reparative processes aimed at restoring impaired functions.

Pathophysiology of Hyperechogenic Bowel in Congenitally Human Cytomegalovirus Infected Fetuses.

Hyperechogenic bowel (HB) is a nonspecific ultrasound finding that can be associated with human cytomegalovirus (CMV) congenital infection. In this study, we investigated HB pathophysiology in CMV-infected fetuses. We examined small and large intestine as well as pancreas in 8 fetuses at 22 weeks of gestation with congenital CMV infection. Ultrasound findings showed 4 fetuses with HB and 4 without. As negative group, 4 fetuses without CMV infection and without HB were studied. Immunohistochemistry for CMV, lymphocytic infiltrate, B-cell leukemia/lymphoma-2 (bcl-2), CD-117, cystic fibrosis transmembrane regulator (CFTR) were performed. HB fetuses showed multiple and sequential CMV-positive ganglion cells of Auerbach’s myenteric plexus. In the ganglia, bcl-2 was weakly expressed representing a reduced neuronal functionality. CD-117 revealed a regular distribution of Cajal cells, the pacemakers of intestinal contractility. Pancreas showed normal CFTR staining, indicating a preserved exocrine secretion, thus unlikely a contributory factor in HB. In CMV-infected fetuses without HB, CMV-positive cells were scatteredly found in ganglion cells and bcl-2 was strongly expressed. Intestinal CD-117 and pancreatic CFTR expression were similar to fetuses with HB. In conclusion, fetal CMV infection of the bowel may lead to peristalsis impairment (paralytic ileus) due to intestinal plexus involvement, which at ultrasound appeared as HB.

Expression of BMP-4 and Smad1 in patients with Hirschsprung disease and its clinical significance.

Expression and clinical significance of bone morphogenetic protein (BMP)-4 and Smad1 in patients with Hirschsprung disease (HD) were investigated. A retrospective analysis of 96 HD patients (experimental group) admitted to Xuzhou Children's Hospital, Xuzhou Medical University from June 2015 to June 2017 was performed. According to the samples, the experimental group was divided into the stenosis group, the transition group and the expansion group. Forty-seven children with colostomy due to intestinal obstruction were selected as the control group. The expression levels of BMP-4 and Smad1 proteins were detected by immunohistochemical staining. The expression levels of BMP-4 and Smad mRNA were detected by real-time quantitative PCR (RT-qPCR), and were quantified and compared. Via immunohistochemistry, BMP-4 and Smad1 proteins were detected in the samples of different parts of HD patients and children with intestinal obstruction. The positive expression levels of BMP-4 and Smad1 proteins in the transition group were decreased compared with those in the expansion and control groups (P<0.05), and the positive expression levels of BMP-4 and Smad1 proteins in the stenosis group were decreased compared with those in the transition, expansion, and control groups (P<0.05). Also, the gene expression levels of BMP-4 and Smad1 in the transition and stenosis groups were successively decreased, and the differences were statistically significant (P<0.05). In conclusion, the expression of BMP-4 and Smad1 in the intestinal plexus of HD lesions was significantly reduced, indicating that BMP-4 and Smad1 are closely related to the occurrence of HD, and it is suspected that they have a certain influence on the intestinal development of congenital digestive tract malformations.

Serotonergic mechanisms of regulation of the systemic circulation vessels lumen

Review is devoted to the assessment of the serotonergic mechanisms role in the hemodynamics regulation. The special attention is given to the role of various serotonin receptors involved in the gastrointestinal tract motility regulation, in particular located in the digestive system vessel walls. It is known that serotonin has a dual effect on the vessel lumen, due to the heterogeneity of serotonin receptors, which are part of the vascular wall, and different sensitivity of serotonin receptors. Mechanisms at various levels, from central to local, are able to participate in the serotonergic regulation of the vascular lumen, as well as in motility control. According to our data, in the regulation of the upper gastrointestinal tract motor activity participate 5-HT1B- and 5-HT3-receptors located in the stomach and intestines autonomic ganglia, 5-HT2B-receptors localized on stomach plexus neurons and on small and large intestine smooth muscles; 5-HT4-receptors located on stomach wall smooth muscles and intraorgan intestinal plexus neurons. According to the literature, vascular wall 5-HT2B- and 5-HT7-receptors provide vasodilation, whereas the 5-HT1B/1D-, 5-HT2A- and 5-HT2B-receptors - vasoconstriction. Significance of plasma free serotonin level for hemodynamic, serotonergic mechanisms for the different types vessels diameter changing, the interaction of serotonin receptors with sympathetic nervous system and their possible role in the vascular tone regulation are described, particularly the role of presynaptic 5-HT1B/1D-receptors, which prevent the catecholamines release by vegetative nerves endings, is established. Different points of view on the serotoninergic regulation issue, existing contradictions, as well as areas for further fundamental and practical research are presented.

Transmural Ileal Ganglioneuromatosis in a Young Boer Goat (Capra hircus)

A diagnosis of transmural ileal ganglioneuromatosis was made in a 15-day-old goat that was found dead following a period of diarrhoea and inappetence. Grossly, the entire length of the wall of the ileum was pale and firm with a variably segmental to transmural thickening. Microscopically, the ileal transmural thickening was due to a diffuse proliferation of both ganglionic and glial cells forming cell nests or packets that infiltrated the wall and into the mesentery surrounding a mesenteric lymph node. The neoplastic ganglionic cells were immunoreactive for S100, synaptophysin and triple neurofilament, while the glial spindle cells were immunoreactive with glial fibrillary acidic protein, S100 and laminin confirming their Schwann cell identity. Nerve fibres expressing neurofilament protein 200 and phosphorylated neurofilament (SMI-31) were observed rarely. Ganglioneuromatosis is defined as diffuse exuberant proliferation of all components of the intestinal ganglionic plexuses. In man, the transmural form has more grave clinical consequences than a focal pattern and is commonly associated with germline mutations in the RET proto-oncogene. Whether there is any comparable molecular genetic abnormality in animals remains unknown; however, ganglioneuromatosis needs to be included in the differential diagnosis of tumours of the autonomic enteric nervous system.

Changes in vasoactive intestinal peptide, pituitary adenylate cyclase-activating polypeptide and neuropeptide Y-ergic structures of the enteric nervous system in the carcinoma of the human large intestine.

This investigation was aimed at immunohistochemical analysis of potential changes in the enteric nervous system caused by cancer of the large intestine. In this purpose, neurons and nerve fibers of intestinal plexuses containing neuropeptides: vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating polypeptide (PACAP) and neuropeptide Y (NPY), in pathologically changed part of the large intestine were microscpically observed and compared. Samples were taken from patients operated due to cancer of the sigmoid colon and rectum. The number of neurons and density of nerve fibres containing neuropeptides found in sections with cancer tissues were compared to those observed in sections from the uninvolved intestinal wall. Changes relating to reductions in the number of NPY-ergic neurons and density of nerve fibres in submucous and myenteric plexuses in the sections with cancer tissues (pathological sections) were statistically significant. A statistically similar presence of VIP-ergic and PACAP-ergic neurons in the submucosal and myenteric plexuses was observed in both the pathological and control sections. On the other hand, in the pathological sections, VIP-ergic nerve fibres in the myenteric plexuses and PACAP-ergic nerve fibres in the submucosal and myenteric plexuses were found to be less dense. Analysis revealed changes in pathologically affected part of the large intestine may caused disruption of proper intestinal function. Observed changes in the neural elements which are responsible for relaxation of the intestine may suggest dysfunction in the innervation of this part of the colon.

The immunohistochemical expression profile of osteopontin in normal human tissues using two site-specific antibodies reveals a wide distribution of positive cells and extensive expression in the central and peripheral nervous systems

To elucidate the cellular distribution of osteopontin (OPN) in normal human tissues, we undertook immunohistochemistry using two site-specific OPN antibodies. The 10A16 monoclonal antibody was raised against the amino acid sequence just downstream of the thrombin cleavage site, while the O-17 polyclonal antibody was raised against the N-terminal peptide. Each antibody has been confirmed previously to react with both whole OPN and its relevant fragments. The expression pattern for these two antibodies was similar in distribution. In addition, we also identified expression in Ebner's gland, type II pneumocytes, Kupffer cells, cells of the endocrine organs, anterior lens capsule and ciliary body, synovial type A cells, mesothelia, adipocytes, and mast cells. Neurons and glia in the central nervous system and spinal cord, cranial and peripheral nerve sheaths, ganglion cells in the sympathetic ganglion, intestinal plexuses, retina, and choroid plexus also regularly exhibited OPN positivity. Testicular germ cells, pancreatic exocrine cells, and follicular dendritic cells reacted with 10A16 only, whereas lutein cells and taste bud cells exhibited O-17 reactivity alone. These minor differences were hypothesized to reflect the state of OPN in the cells; that is, whether OPN was in its whole molecule or fragmented form. In conclusion, we demonstrate that OPN is widely distributed in normal human cells, particularly those comprising the central and peripheral nervous systems.

Syncytial coupling of neurons in tissue culture and early ontogenesis

Computerized time-lapse video recording was used to detect the process of formation of syncytial couplings between the processes of different neurons in dissociated neuron cultures. These studies showed that once the processes of one neuron had formed connections with another neuron, death of the cell body (its trophic center) was not followed by Wallerian degeneration. Translocation of cytoplasmic varicosities along the branches of one neuron to another was observed over periods of several hours. Electron microscopic studies of the nerve processes of cells in the intramural intestinal plexus in the early postnatal period demonstrated all the transitional states from fusion and perforation of the membranes of contacting dendrites to complete fusion of the neuroplasm of processes with formation of residual membranous structures at the location of the former intercellular contact.

Megacolon in an Adult Case of Hypoganglionosis, a Pseudo-Hirschsprung's Disease: An Autopsy Study

We report an autopsied 20-year-old man case of intestinal necrosis associated with megacolon from hypoganglionosis, a pseudo-Hirschsprung's disease. The patient had suffered from severe constipation since two years of age, and presented abdominal distention from age ten. Autopsy revealed marked dilatation and necrosis of the entire large intestine. Although ganglion cells in the intestinal plexus were found throughout the large intestine, their number was reduced to 12-20% of that in the normal control. In pseudo-Hirschsprung's disease, there are occasional cases where an acute abdomen first presents itself in adulthood after running its course as chronic constipation.

Metabotropic signal transduction for bradykinin in submucosal neurons of guinea pig small intestine.

Intracellular recording methods with "sharp" microelectrodes were used to study signal transduction mechanisms underlying the excitatory action of bradykinin (BK) in morphologically identified neurons in the small intestinal submucosal plexus. Exposure to BK evoked slowly activating membrane depolarization and enhanced excitability associated with increased input resistance in AH-type and decreased input resistance in S-type neurons. Preincubation with pertussis toxin did not affect the BK-evoked responses. Pretreatment with the cyclooxygenase inhibitors indomethacin or piroxicam suppressed or abolished the BK-evoked responses. Application of prostaglandin (PG) E(2) or PG analogs evoked BK-like depolarizing responses in the submucosal plexus with a potency order of PGE(2) > PGE(1) > 17-phenyl trinor-PGE(2) > PGI(2) > sulprostone > PGF(2alpha). Depolarizing responses to bradykinin or PGE(2) in S-type neurons were suppressed in the presence of the phospholipase C inhibitor U73122 [(1-6-[([17beta]-3-methoxyestra-1,3,5[10]-tren-17-71)amino]hexyl)-1H-pyrrole-2,5-dione)], but not the inactive analog U73343 [(1-6-[([17beta]-3-methoxyestra-1,3,5[10]trien-17yl)amino]hexyl)-2,5-pyrrolidinedione)]. The inositol-1,4,5-trisphosphate receptor antagonist 2-aminoethoxy-diphenylborane and the calmodulin inhibitor W-7, but not ryanodine, suppressed both bradykinin- and PGE(2)-evoked responses. KN-62, an inhibitor of calmodulin kinases, or GF109203X, a specific protein kinase C inhibitor, suppressed both BK- and PGE(2)-evoked depolarizing responses. Selective protein kinase A inhibitors did not alter BK- or PGE(2)-evoked depolarizing responses in S neurons. The results suggest that BK stimulates synthesis and release of PGE(2), which acts at EP(1) receptors to evoke depolarizing responses in submucosal neurons. The postreceptor transduction cascade includes activation of phospholipase C, inositol-1,4,5-trisphosphate production, intraneuronal Ca2+ mobilization, activation of protein kinase C and/or calmodulin kinases, and phosphorylation of cationic channels.

Persistence of abnormal gastrointestinal motility after operation for Hirschsprung’s disease

OBJECTIVE: Recent studies in patients with Hirschsprung’s disease (HD) suggest that morphological abnormalities of the intramural intestinal plexuses are not restricted to the colon. In this report, symptoms and objective tests of gastrointestinal (GI) motor dysfunction were determined long after operative treatment to see whether evidence of a more widespread and relevant motility disturbance could be detected. METHODS: Twenty-one children were available for study an average of 6.6 yr after surgery for HD. All of these patients underwent evaluation of bowel frequency per week, total GI transit time (TGTT), and a scintigraphic gastric emptying test using solid food; anorectal manometry and segmental colonic transit times were performed in a subset of patients. Results were compared with findings in appropriately matched controls. RESULTS: Frequency of defecation per week in patients with HD after surgery was not different from that in control children, but TGTT was significantly longer ( p < 0.01). Percentage retention of gastric isotope at 60 min exceeded the normal range in 12 of 21 (57.1%) patients, and colonic transit was abnormal in all six children studied. Symptoms persisted in two-thirds of patients postoperatively, and transit abnormalities were more common in the symptomatic subset ( p = 0.026). CONCLUSIONS: Our data show that, in a subset of patients with HD, GI motor dysfunction persists long after surgical correction. The heterogeny of basic defects responsible for HD could provide the substrate for these motor abnormalities that, in turn, seem at least partially responsible for continuation of the symptomatic state.

Persistence of abnormal gastrointestinal motility after operation for Hirschsprung's disease.

Recent studies in patients with Hirschsprung's disease (HD) suggest that morphological abnormalities of the intramural intestinal plexuses are not restricted to the colon. In this report, symptoms and objective tests of gastrointestinal (GI) motor dysfunction were determined long after operative treatment to see whether evidence of a more widespread and relevant motility disturbance could be detected. Twenty-one children were available for study an average of 6.6 yr after surgery for HD. All of these patients underwent evaluation of bowel frequency per week, total GI transit time (TGTT), and a scintigraphic gastric emptying test using solid food; anorectal manometry and segmental colonic transit times were performed in a subset of patients. Results were compared with findings in appropriately matched controls. Frequency of defecation per week in patients with HD after surgery was not different from that in control children, but TGTT was significantly longer (p < 0.01). Percentage retention of gastric isotope at 60 min exceeded the normal range in 12 of 21 (57.1%) patients, and colonic transit was abnormal in all six children studied. Symptoms persisted in two-thirds of patients postoperatively, and transit abnormalities were more common in the symptomatic subset (p = 0.026). Our data show that, in a subset of patients with HD, GI motor dysfunction persists long after surgical correction. The heterogeny of basic defects responsible for HD could provide the substrate for these motor abnormalities that, in turn, seem at least partially responsible for continuation of the symptomatic state.

Endoscopic polypectomy of an unusually long polypoid colorectal cavernous hemangioma

phages, and they are converted to lipofuscin as macrophages migrate to the lamina propria of the mucosa.3,4 Moreover, results in animal experiments have suggested that long-term administration of anthraquinone cathartics not only causes changes in the intestinal mucosa but also affects the intestinal plexuses to further aggravate constipation.5 Bamboo leaf extract, which is prepared primarily from leaves of kumaisasa, is sold as a dark green fluid. There have been reports that lignin, one of its components, exhibited anti-tumor effects in animals bearing benzopyrene-induced and 4-nitroquinoline-1-oxide (4NOQ)-induced tumors6 and that it alleviated alcoholic fatty liver in rats.7 In acute and subacute toxicity studies, impaired liver and kidney functions were observed in rats given lignin at high doses.8 Because bamboo leaf extract was not ordinarily ingested by humans, the possibility of its deposition in the intestinal mucosa has not been considered. There have been no reports on the safety of its long-term administration, and the question remains open. The evidence in this report is circumstantial as the patient was not rechallenged, but dose suggest a possible association between Melanosis coli and ingestion of bamboo leaf extract. There may be differences between the histologic changes induced by anthraquinone laxatives and bamboo leaf extract although no firm conclusion can be reached based on study of a single patient.

Neurturin and Glial Cell Line-Derived Neurotrophic Factor Receptor-β (GDNFR-β), Novel Proteins Related to GDNF and GDNFR-α with Specific Cellular Patterns of Expression Suggesting Roles in the Developing and Adult Nervous System and in Peripheral Organs

Cloning strategies were used to identify a gene termed glial cell line-derived neurotrophic factor receptor-beta (GDNFR-beta) related to GDNFR-alpha. In situ hybridization was then used to map cellular expression of the GDNF-related trophic factor neurturin (NTN) and GDNFR-beta mRNA in developing and adult mice, and comparisons with GDNFR-alpha and RET were made. Neurturin is expressed in postnatal cerebral cortex, striatum, several brainstem areas, and the pineal gland. GDNFR-beta mRNA was more widely expressed in the developing and adult CNS, including cerebral cortex, cerebellum, thalamus, zona incerta, hypothalamus, brainstem, and spinal cord, and in subpopulations of sensory neurons and developing peripheral nerves. NTN colocalized with RET and GDNFR-alpha in ureteric buds of the developing kidney. The circular muscle layer of the developing intestines, smooth muscle of the urether, and developing bronchiolae also expressed NTN. GDNFR-beta was found in myenteric but not submucosal intestinal plexuses. In developing salivary glands NTN had an epithelial expression, whereas GDNFR-beta was expressed in surrounding tissue. Neurturin and GDNFR-beta were present in developing sensory organs. In the gonads, NTN appeared to be expressed in Sertoli cells and in the epithelium of the oviduct, whereas GDNFR-beta was expressed by the germ cell line. Our findings suggest multiple roles for NTN and GDNFR-beta in the developing and adult organism. Although NTN and GDNFR-beta expression patterns are sometimes complementary, this is not always the case, suggesting multiple modi operandi of GDNF and NTN in relation to RET and the two binding proteins, GDNFR-alpha and GDNFR-beta.

Galanin-like immunoreactivity in the sea cucumber Holothuria glaberrima.

Galanin, a neuropeptide of 29 amino acids originally purified from porcine small intestine, has been found in most vertebrate groups, where it is present in both the central and peripheral nervous systems. In this study, galanin-like immunoreactivity was detected in an invertebrate, the sea cucumber Holothuria glaberrima. In this organism, fibers and cells expressing galanin-like immunoreactivity were found in the enteric nerve plexuses of the esophagus, and large and small intestine, particularly in the serosal layer. Immunoreactivity was also found in the ectoneural portion of the radial nerve and in nervous elements within the body wall. Preabsorbtion tests indicated that the observed immunoreactivity was not due to cross-reactivity of the antibody with other peptides also found in the intestinal plexuses. The immunoreactivity to galanin was quantified in various tissues using radioimmunoassay and partially characterized with high performance liquid chromatography. These results show that although the holothurian peptide shows common immunological determinants with porcine galanin, it differs with regard to certain biochemical properties.

Immunohistochemical localization of RET protein in Hirschsprung's disease

A major gene causing Hirschsprung's disease was recently mapped in 10q11.2. Its physical localization was restricted to a 250-Kb interval containing the RET protooncogene (REarranged during Transfection). In 1994, point mutations affecting the RET proto-oncogene were identified in patients with Hirschsprung's disease. The authors present an immunohistochemical study on the expression and localization of the Ret protein (a receptor tyrosine kinase, which is the RET proto-oncogene product) in the intestinal plexuses of patients with Hirschsprung's disease. Ninety-two full-thickness intestinal wall pieces from 29 pediatric patients were studied (19 cases of classic Hirschsprung's disease, 5 of total colonic aganglionosis, and 5 controls). Ret protein immunohistochemical localization was obtained using c-Ret R5, anti-Ret K and anti-Ret C antibodies, respectively, against the extracellular domain, the tyrosine kinase domain, and the carboxy-terminal 20 amino acids of the Ret protein. A diffuse granular staining was present in the ganglia of normal colon, whereas the small ganglia of the hypoganglionic colon showed a reduced number of ganglion cells that were strongly stained with c-Ret R5 MoAb. A reduced synthesis of Ret protein was shown in the ganglionic and hypoganglionic segments of two cases of this series, the first with a complete deletion of the RET proto-oncogene and the second with a frameshift mutation and a stop codon in the extracellular domain. The activity of the receptor tyrosine kinases (RTKs) in intestinal ganglion cells was investigated using antiphosphotyrosine antibodies. A very low tyrosine kinase activity was shown in the small ganglia of the hypoganglionic segment. The results of this study suggest a primary role of this transmembrane receptor in the migration and differentiation of neural crest-derived neuroblasts that colonize the colon. The identification of the Ret protein ligand will better explain the role of this transmembrane receptor in the molecular and cellular mechanisms of Hirschsprung's disease.

Electrophysiological properties of neurons in submucosal ganglia of guinea pig distal colon

Intracellular recording methods were used in vitro to study the electrophysiological behavior of neurons in ganglia of the submucosal plexus in the distal colon of the guinea pig. The results revealed subpopulations of submucosal ganglion cells that corresponded to the AH/type 2, S/type 1, type 3, and type 4 subpopulations found elsewhere in the intestine. Electrical behavior of colonic submucosal neurons differed from the myenteric plexus of the colon, rectum, and stomach and the small intestinal submucosal plexus mainly in the relative proportions of the different subpopulations. Regional differences in this respect may be a reflection of functional specialization in the diverse regions of the alimentary canal.

Immunological quantitation and immunohistochemical localization of leukotriene A4 hydrolase in guinea pig tissues.

We prepared a highly specific polyclonal antibody against leukotriene (LT) A4 hydrolase using a recombinant human enzyme. Using this antibody, we quantified LTA4 hydrolase protein content in the cytosols of guinea pig tissues. The enzyme protein content correlated well with the enzyme activity with a correlation coefficient of 0.87. However, the enzyme activity per mg of the enzyme in the cytosols was low, particularly in the liver and adrenal gland, compared with the specific activity of the purified enzyme. These observations suggest the presence of inhibitory substances and/or inactive enzymes in the cytosols of these tissues. To determine the cellular localization of LTA4 hydrolase in tissues other than blood cells, we carried out immunohistochemical examinations of guinea pig tissues. We identified epithelial cells in the tracheobronchial system and gastrointestinal tract, smooth muscle cells in the bronchi and aorta, vascular endothelial cells, and the intestinal plexus as novel cellular sources of the enzyme in the parenchyme of the tissue. Thus, LTA4 hydrolase was widely distributed in various types of parenchymal cells in the tissues, and this observation warrants further investigations on the biological activities of LTB4 in these cells and tissues.

Intestinal plexuses in Crohn's disease and ulcerative colitis in children: pathologic and microdissection studies.

The relative fraction of neural tissue in the plane of the myenteric (Auerbach) plexus (MEP) of ileum and colon of patients with Crohn's disease and ulcerative colitis was analyzed by point-count morphometric analysis of microdissected flat-mount ("circuit diagram") preparations of the plexus. Increase in the relative fraction of neural tissue (myenteric plexus hyperplasia) was seen in the MEP of some patients in both ileum and colon in both diseases. The frequency of ulceration or inflammation extending into the bowel wall deep enough to injure the various levels of the intestinal plexus system (mucosal plexus of Cajal; upper submucosal plexus of Meissner; deeper submucosal plexus of Henle; intermuscular plexus of Auerbach; outer muscular/serosal plexus of Stöhr) was analyzed for small intestine, appendix, and colon for patients with both diseases. As expected, Crohn's disease tends to produce deeper intestinal wall damage in ileum versus colon, and ulcerative colitis the reverse. The effect of such injury on local and more distal motor control of the intestine and on integrative functions of the intestinal plexus system appears not to have been considered previously. Since injury deep enough to damage any given plexus necessarily damages all overlying plexus levels, analysis of such effects appears a fruitful field for study.

Rôle du système nerveux autonome dans la régulation du transit, de l'absorption et du stockage des nutriments

The possible role of the autonomic nervous system (ANS) in nutrition must be reevaluated in view of recent experimental data. The ANS plays a major part in both initiating and maintaining peristalsis and in coordinating gastrointestinal motility. Intestinal absorption involves extra-epithelial mechanisms such as motility and vasomotricity of the digestive tract. In addition, the ANS (sympathetic fibres) might act directly on enterocytes, or indirectly via the intestinal plexuses through a glucose-dependent mechanism. The control of exocrine and endocrine secretions depends partly on the ANS. In particular the mucous mechanoreceptors, chemoreceptors and thermoreceptors located in the intestinal area supply the sensory information needed in that kind of regulation. The efferent fibres of the ANS intervene in the control of storage of carbohydrates in the liver and of lipids in brown adipose tissue. On the other hand, gastrointestinal afferents might be implicated in this mechanism through the hypothalamic ventro-median nucleus. Finally, these data are consistent with a modern conception suggesting that the ANS is largely involved in the regulation of visceral motility, homeostasis and alimentary behaviour.