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PubMed2003

Embryonic development of the myenteric nerve plexus in the rat small intestine as revealed by light and scanning electron microscopy.

This study was performed to clarify developmental changes in the structure of the myenteric nerve plexus in the rat small intestine. The small intestines of fetal and neonatal rats were examined by light microscopic immunohistochemistry for protein gene product 9.5 (PGP-9.5) and alpha-smooth muscle actin (alpha-SMA). Direct observation of the three-dimensional structure of the neuronal and muscular elements was accomplished by scanning electron microscopy of tissues after KOH treatment. At the embryonic day 14 (E14), PGP-9.5 immunopositive (neuronal) cells first appeared in the mesenchymal tissue outside an alpha-SMA positive (muscle) cell layer. These cells increased in number to form a thin and continuous sheet, which was sandwiched between the inner and outer muscular layers at E17. This neuronal layer consisted of immature ganglion cells associated with supportive (enteroglial) cells, and was gradually segregated into groups by incomplete separation through slit-like interruptions at E18. With the widening of these slits at E19, the neuronal sheet was observed as a ladder composed of transversely elongated ganglia and their connecting nerve strands, resulting in the typical structure of the myenteric nerve plexus. Fibroblastic cells of a peculiar shape appeared on the outer surface of the myenteric plexus at E19. These cells (presumably interstitial cells) interconnected their long branching projections to form a cellular network on the myenteric plexus until birth.

Animals↗

PubMed2003

Nitrergic hyperinnervation in appendicitis and in appendices histologically classified as normal.

CONTEXT: The pathogenesis of appendicitis remains poorly understood. Despite new diagnostic techniques, appendices removed from patients with suspected appendicitis often appear histologically normal on conventional examination. There is increasing evidence of involvement of the enteric nervous system in immune regulation and in inflammatory responses in the gastrointestinal system. OBJECTIVE: To investigate the nitrergic innervation of (a) acutely inflamed appendices, (b) appendices classified as histologically normal from patients with a clinical diagnosis of appendicitis, and (c) normal control appendix specimens, using the whole-mount preparation technique. PATIENTS AND DESIGN: Full-thickness specimens were collected from 28 acutely inflamed appendices (age range, 3.2-13.4 years), 31 histologically normal appendices removed from patients (age range, 5.7-13.6 years) with suspected appendicitis, and 23 histologically normal appendices from patients (age range, newborn to 12.1 years) undergoing elective abdominal surgery (controls). Whole-mount preparation using nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemistry and neuronal nitric oxide synthase immunohistochemistry were performed. The density of myenteric plexus was measured with a computerized analysis system. RESULTS: The density of myenteric plexus in normal appendix specimens was similar to that of large bowel from the newborn period up to 3 years of age; this density decreased significantly thereafter. The myenteric plexus of normal appendix specimens from patients older than 4 years demonstrated smaller ganglia connected by thin nerve bundles, compared to larger ganglia and nerve bundles in large bowel. Significant neuronal hypertrophy was found in 55% of acutely inflamed and 41% of histologically classified normal appendix specimens. The myenteric plexus of these appendix specimens had even thicker nerve bundles connecting an increased number of ganglion cells. CONCLUSIONS: Differences in the architecture of the myenteric plexus in patients older than 3 years suggest an altered function and motility of appendix in the early years of life. The significant increase in neuronal components of the myenteric plexus in a high proportion of acutely inflamed and histologically normal appendix specimens is unlikely to have developed during a single acute inflammatory episode. This suggests an underlying chronic abnormality as a secondary response to chronic luminal obstruction or repeated inflammatory episodes in the histologically normal appendix.

Adolescent↗

PubMed2003

Protein kinases expressed by interstitial cells of Cajal.

Interstitial cells of Cajal (ICC) are involved in the generation of electrical rhythmicity of intestinal muscle and in the transduction of neural inputs in the gut. Although the expression of receptors for neurotransmitters and hormones and some second messengers have been investigated in ICC, the protein kinases present in these cells have not been well documented. This study has demonstrated the immunohistochemical localisation of PKA, PKC gamma and PKC theta in ICC that were identified by the known ICC marker, c-Kit, in the guinea-pig gut. Other PKCs, PKC alpha, beta, delta, epsilon, eta, iota and lambda, and Ca(2+)-calmodulin-dependent protein kinase II were not localised in ICC. Double labelling studies were conducted on longitudinal muscle-myenteric plexus and external muscle-myenteric plexus preparations of the oesophagus, stomach (fundus, corpus and antrum), duodenum, distal ileum, caecum, proximal and distal colon, and rectum. The three protein kinases were detected in c-Kit-immunoreactive ICC at the level of the myenteric plexus (IC-MY), in the muscle (IC-IM) and at the level of the deep muscular plexus (IC-DMP) in the small intestine. PKA was found in over 90% of IC-IM in all regions examined, and in over 90% of IC-MY in the gastric body and antrum and throughout the small and large intestines. PKC gamma was in the majority of ICC in the gastric body and antrum and in the small intestine, but was largely absent from ICC in the oesophagus, proximal stomach and large intestine. PKC theta occurred in the majority of ICC in all regions except the rectum. The intensity of staining was greatest for PKA, with PKC gamma giving comparatively weak labelling of ICC. PKA was also detected in myenteric neurons, smooth muscle, macrophages and fibroblast-like cells. PKC gamma labelling occurred in large, multipolar neurons throughout the small and large intestine, as well as in lymph vessels and in capillaries. It is concluded that PKA, PKC gamma and PKC theta are all present in ICC, with the differences in their localisations suggesting specific roles for each in ICC function.

Animals↗

PubMed1979

Projections of intestinal neurons showing immunoreactivity for vasoactive intestinal polypeptide are consistent with these neurons being the enteric inhibitory neurons.

Experiments were performed to determine if the distribution of vasoactive intestinal peptide(VIP)-like immunoreactivity in nerve cell bodies and axons of the myenteric plexus and circular muscle of the small intestine is consistent with VIP being the transmitter of enteric inhibitory neurons. Immunoreactivity for VIP was found in nerve cell bodies of the myenteric plexus and in axons within the myenteric plexus and circular muscle. When the axons in the myenteric plexus were interrupted, there was accumulation of material showing reactivity for VIP on the oral side, indicating that the neurons project in an anal direction. The VIP-like immunoreactivity in axons which supply the circular muscle disappeared after a myectomy in which the overlying myenteric plexus was removed, but remained intact when extrinsic nerves were served. The projections of VIP neurons from the myenteric plexus to the circular muscle correspond to the expected projections of enteric inhibitory neurons determined by functional studies.

Animals↗

PubMed1986

Ultrastructure and localization of substance P and met-enkephalin immunoreactivity in the human fetal gastric antrum.

The ultrastructural localization and relations of substance P- and met-enkephalin-labeled neuronal structures were examined in the wall of the human gastric antrum during early fetal life. By 14-16 weeks of gestation, clearly discernable neural plexuses and a well developed external muscle coat were present. In the submucous coat, neural plexuses varied from immature forms consisting of 1-4 neurites partially enveloped by Schwann cell processes to more mature plexuses where neurons were completely enclosed by Schwann cell processes. Neuronal profiles with substance P- and met-enkephalin-like immunoreactivities were observed in the submucous plexus. In the myenteric plexus met-enkephalin-like immunoreactivity was seen within cell bodies and neurites. By contrast, although substance P-like immunoreactivity was observed in neurites in the myenteric plexus, no substance P-labeled somata could be identified. Unlabeled terminals were seen in contact with both unlabeled dendrites and met-enkephalinergic neurons. An increase in electron density was observed at the sites of contact. These structures probably represent early stages in the development of synaptic specializations. In addition, met-enkephalin-labeled varicosities were seen in apposition to smooth muscle cells of the circular muscle coat. This suggests that antral smooth muscle cells are directly innervated by met-enkephalin neurons.

Embryonic and Fetal Development↗

PubMed1989

A model for aganglionosis in the chicken embryo.

We investigated the ability of neural crest (NC) cells to colonize hindgut, which had remained aneuronal due to bowel transection in ovo at an early stage. The fact that the bowel remained aneuronal proved that the "sacral" NC does not provide precursor cells for enteric neurons in the hindgut. HNK-1 immunostaining of aneuronal hindgut revealed cell-free, ganglionic structures at the site of the myenteric plexus and a sub-population of mesenchymal cells in the submucosa. We cocultured this particular type of aneuronal bowel with the vagal neural anlage of either quail or chick embryos on the chick chorioallantoic membrane. After 1 week coculture, it appeared that NC cell colonisation of the hindgut had taken place, although there was a difference between the quail-chick and chick-chick model. Quail NC cells had given rise to submucous plexuses and some myenteric plexuses. Chick NC cells had only colonised the submucous region. These findings indicate that the cell-free ganglionic structures hamper neural crest cell colonization in the myenteric region.

Animals↗

PubMed2004

The opioid system in the gastrointestinal tract.

Mu-, delta- and kappa-opioid receptors (ORs) mediate the effects of endogenous opioids and opiate drugs. Here we report (1) the distribution of muOR in the guinea-pig and human gastrointestinal tract in relation to endogenous ligands, to functionally distinct structures in the gut and to deltaOR and kappaOR; and (2) the ligand-induced muOR endocytosis in enteric neurones using in vitro and in vivo models. In the guinea pig, muOR immunoreactivity is confined mainly to the myenteric plexus. MuOR myenteric neurones are most numerous in the small intestine, followed by the stomach and the proximal colon. MuOR immunoreactive fibres are dense in the muscle layer and the deep muscular plexus, where they are in close association with interstitial cells of Cajal. This distribution closely matches the pattern of enkephalin. MuOR enteric neurones comprise functionally distinct populations of neurones of the ascending and descending pathways of the peristaltic reflex. In human gut, muOR immunoreactivity is localized to myenteric and submucosal neurones and to immune cells of the lamina propria. DeltaOR immunoreactivity is located in both plexuses where it is predominantly in varicose fibres in the plexuses, muscle and mucosa, whereas kappaOR immunoreactivity appears to be confined to the myenteric plexus and to bundles of fibres in the muscle. MuOR undergoes endocytosis in a concentration-dependent manner, in vitro and in vivo. Pronounced muOR endocytosis is observed in neurones from animals that underwent abdominal surgery that has been shown to induce delay in gastrointestinal transit. We can conclude that all three ORs are localized to the enteric nervous system with differences among species, and that muOR endocytosis can be utilized as a means to visualize enteric neurones activated by opioids and sites of opioid release.

Adult↗

PubMed1985

Three serial neurones in the innervation of the colon by the sacral parasympathetic nerve of the dog.

Electrophysiological and histological techniques were used to study the nature of the innervation of the colon by the sacral parasympathetic nerve of the dog. Many cells which incorporate horseradish peroxidase (HRP) were observed in ganglia of the pelvic plexus, but not in the sacral cord, after HRP was injected into the wall of the distal colon. Stimulation of the pelvic ganglia by an application of dimethylphenylpiperazinium contracted the distal colon. The contraction was reduced by nicotine applied to the colon. Compound action potentials in responses of rectal strands of the pelvic nerve to stimulation of the sacral ventral roots decreased or disappeared after hexamethonium bromide (C6) was applied to the pelvic plexus. Conduction velocities of the potentials showed that most of the preganglionic fibres were B fibres, and nearly all the post-ganglionic fibres were C fibres. Many C fibres were observed by electron microscopy in the rectal strands after degeneration of the pelvic and hypogastric nerves. Stimulation of such rectal strands caused a contraction of the colon, which diminished after C6 was applied to the distal colon. These results show that the sacral parasympathetic nerve innervating the colon comprises three serial neurones located in the sacral spinal cord, the pelvic plexus and the myenteric plexus.

Action Potentials↗

PubMed1985

Slow wave heterogeneity within the circular muscle of the canine gastric antrum.

A cross-sectional preparation was designed in which multiple micro-electrodes can be precisely positioned to impale smooth muscle cells anywhere from the serosa to the submucosa. Intracellular electrical recordings were obtained from gastric antral circular muscle cells from the myenteric plexus to the submucosa. The resting membrane potential changed linearly as a function of distance from the myenteric plexus to the submucosa. Slow wave upstroke dV/dt, upstroke potential amplitude, and plateau potential amplitude changed linearly as a function of distance from the myenteric plexus to the submucosa. When slow waves were recorded simultaneously from a circular cell near the myenteric plexus and from a cell near the submucosa, the event always occurred first in the cell near the myenteric plexus. Electrical differences did not appear to be caused by electrotonic decay of slow waves as they propagated through the circular muscle. Electrical differences could not be explained on the basis of differences in intrinsic neural activity or prostaglandin synthesis. Membrane polarization could not explain the differences in slow waves between myenteric and submucosal circular muscle cells. The conclusion of this paper is that fundamental differences exist between the excitability mechanisms and/or passive membrane properties of cells near the myenteric plexus and the submucosa. These differences might be manifest in different motor performance of these two muscle cell populations.

Action Potentials↗

PubMed1991

Inhibition of acetylcholine release from guinea pig myenteric neurons by neuropeptide Y: GTP-binding protein mediation.

Neuropeptide Y (NPY) is a unique peptide with wide distribution in central and peripheral nervous systems. In the guinea pig, NPY-positive fibers are prominent in the myenteric plexus. To test whether NPY inhibits myenteric plexus acetylcholine (ACh) release and to define mechanisms, a purified preparation of myenteric plexus neurons was derived from the teniae coli of neonatal guinea pigs and maintained in primary culture. Incubation of cultured neurons labeled with [3H]ACh in the presence of NPY (10(-14)-10(-6) M) significantly inhibited basal ACh release (83 +/- 16 to 58 +/- 11% of control). NPY significantly inhibited ACh release stimulated by potassium (55 mM); by adenylate cyclase agonists forskolin (10(-6) M) and cholera toxin (10(-8) M); and by calcitonin gene-related peptide, cholecystokinin octapeptide, and vasoactive intestinal peptide (each 10(-8) M). In each instance, the inhibitory effects of NPY were reversed by preincubation with pertussis toxin. Reversal of inhibitory effects by pertussis toxin suggests that the actions of NPY are mediated via an inhibitory GTP-binding protein.

Acetylcholine↗

PubMed1993

Distribution of VIP-immunoreactive nerve cells and fibers in the human ileocecal region.

VIP-containing nerve cells and fibers in the human ileocecal region (pre-junctional ileum, ileocecal and cecocolonic junctions, post-junctional cecum and colon) have been evaluated by immunocytochemistry. A high density of VIP-positive neurons and nerve fibers was found in all layers of the ileum. At all colonic levels examined and at both junctions, the percentage of VIP-containing cells was higher in the submucous plexus than in the myenteric plexus. At both junctions, the muscle wall was devoid of, and the myenteric plexus extremely poor in VIP-positive nerve fibers and cells. These data suggest that motility of these junctions is not--or only to a minor extent--regulated in man by VIP-containing nerves, at variance with other gut sphincteric areas.

Cecum↗

PubMed2001

Morphometry of submucous and myenteric esophagic plexus of dogs experimentally reinfected with Trypanosoma cruzi.

We carried out a morphometric study of the esophagus of cross-bred dogs experimentally infected or consecutively reinfected with Trypanosoma cruzi 147 and SC-1 strains, in order to verify denervation and/or neuronal hypertrophy in the intramural plexus. The animals were sacrificed in the chronic stage, 38 months after the initial infection. Neither nests of amastigotes, nor myositis or ganglionitis, were observed in all third inferior portions of esophageal rings analyzed. No nerve cell was identified in the submucous of this organ. There was no significant difference (p>0.05) between the number, maximum diameter, perimeter, or area and volume of the nerve cells of the myenteric plexus of infected and/or reinfected dogs and of the non-infected ones. In view of these results we may conclude that the 147 and SC-1 strains have little neurotropism and do not determine denervation and/or hypertrophy in the intramural esophageal plexuses in the animals studied, independent of the reinfections.

Animals↗

PubMed2006

Expression and significance of nerve growth factor receptor p75 in rats' cathartic colonic wall.

OBJECTIVE: To investigate the expression of nerve growth factor receptor p75 in a normal and cathartic colon and its significance in the formation of the cathartic colon in rats. METHODS: Sixty Sprague-Dawley rats were equally divided into normal control group, rhubarb group and phenolphthalein group. A model of the cathartic colon was constructed by gastric infusion with rhubarb or phenolphthalein in rats. The first dose of rhubarb and phenolphthalein was both 200 mg/kg/d and was increased by 200 mg/kg/d with each passing day. The last dose of rhubarb and phenolphthalein was 3200 mg/kg/d and 4200 mg/kg/d, respectively. The transit function of colon was measured by the Chinese ink expulsion test; the p75 in colon wall was determined by the immunohistochemical method. RESULTS: The transit speed was much slower in the cathartic colon group than that in the control group. The imprinted Chinese ink length and the ratio of imprinted length/total colon length in the rhubarb-induced cathartic colon was significantly shorter than that of the control group (77.38 +/- 8.42 vs 94.25 +/- 7.07 cm, P < 0.01). Those in the phenolphthalein-induced group (83.38 +/- 9.75 cm) were also significantly shorter than those of the control group but to a lesser degree (P < 0.05). p75 was abundantly expressed in the submucosal nerve plexus and weakly expressed in the myenteric plexus. The expression of p75 was much higher in the rhubarb-induced group. The expression was strongly positive in the submucosal nerve plexus, significantly higher than that in the controls (P < 0.01). In the myenteric plexus, p75 was also highly expressed (P < 0.05). In the case of the phenolphthalein-induced group, the expression of p75 was positive in the submucosal nerve plexus but was positive in the myenteric plexus of three rats only. The remaining rats were negative or weakly positive. This was not significantly different from that of the control group. CONCLUSIONS: The abnormal expression of p75 in cathartic colon probably has some effect on the degeneration or apoptosis of neuronal cells in the enteric nerve plexus, with a subsequent pathological change of the enteric nervous system, and thus leads to abnormalities in colonic dynamics. The kind of lesion is probably associated with long-term use of irritative cathartics.

Animals↗

PubMed1984

Jejunal diverticulosis with perforation as a complication of Fabry's disease.

This study presents the case of a patient who had jejunal diverticulosis with perforation and abscess formation as a complication of Fabry's disease. Light microscopy disclosed glycolipid deposition in the neurons and nerve fibers of the intestinal nerve plexuses and smooth muscle. Silver stains of the myenteric plexus in the involved segment of the bowel showed enlarged, granular argyrophobic neurons and a marked decrease in the number of argyrophilic neurons, with those remaining being enlarged and distorted by the cytoplasmic glycolipid accumulation. These abnormalities of the myenteric plexus suggest that jejunal diverticulosis may be the result of a variety of disorders of the smooth muscle or myenteric plexus, or both. We propose that jejunal diverticulosis in our patient was a consequence of uncoordinated smooth muscle activity resulting from Fabry's involvement of myenteric plexus neurons, with mucosal protrusion through the smooth muscle.

Abscess↗

PubMed1984

Distribution and projections of neurons with immunoreactivity for both gastrin-releasing peptide and bombesin in the guinea-pig small intestine.

Bombesin-like and gastrin-releasing peptide (GRP)-like immunoreactivities were localized in nerves of the guinea-pig small intestine and celiac ganglion with the use of antibodies raised against the synthetic peptides. The anti-bombesin serum (preincubated to avoid cross reactivity with substance P) and the anti-GRP serum revealed the same population of neurons. Preincubation of the anti-bombesin serum with bombesin abolished the immunoreactivity in nerves while absorption of the anti-GRP serum with either bombesin or the 14-27 C-terminal of GRP only reduced the immunoreactivity. The immunoreactivity was abolished by incubation with GRP 1-27. Immunoreactive nerves were found in the myenteric plexus, circular muscle, submucous plexus and in the celiac ganglion. Faintly reactive nerve cell bodies were found in the myenteric ganglia (3.2% of all neurons) but not in submucous ganglia. After all ascending and descending pathways in the myenteric plexus had been cut, reactive terminals disappeared in the myenteric plexus, circular muscle (including the deep muscular plexus) and the submucous plexus on the anal side. After the mesenteric nerves were cut no changes were observed in the intestinal wall but the reactive fibres in celiac ganglia disappeared. It is deduced that GRP/bombesin-immunoreactive nerve cell bodies in myenteric ganglia project from the myenteric plexus to other myenteric ganglia situated further anally (average length 12 mm), anally to the circular muscle (average length 9 mm), anally to submucous ganglia (average length 13 mm) and external to the intestine to the celiac ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Involvement of enteric neurones in the response of guinea-pig ileum preparations to metoclopramide.

The role of myenteric neurones in mediating the stimulant effects of metoclopramide in vitro in the guinea-pig ileum has been investigated using the non-ionic surfactant Triton X-100. Histological examination of the ileum 30 days after application of Triton X-100 to the serosal surface demonstrated a marked reduction in the number of ganglion cells and nerve elements in the myenteric plexus. Longitudinal muscle-myenteric plexus (LM-MP) preparations from Triton X-100-treated animals were unresponsive to dimethylphenylpiperazinium and responded poorly or not at all to electrical field stimulation. Metoclopramide (30 microM) elicited small contractions in LM-MP preparations from control and sham-operated animals but failed to contract Triton X-100-treated tissues. However, tissues responded in a similar manner to exogenous acetylcholine (ACh). These results demonstrate the importance of a prejunctional site of action for metoclopramide in this tissue and suggest that contractile responses to the drug are mediated indirectly, probably by increased release of ACh from myenteric neurones.

Acetylcholine↗

PubMed1986

Electrophysiological analysis of projections of enteric inhibitory motoneurones in the guinea-pig small intestine.

The projections of neurones that produce inhibitory junction potentials (i.j.p.s) have been analysed in the small intestine of the guinea-pig. Intracellular microelectrodes were used to record i.j.p.s in circular muscle cells in response to stimulation with pairs of electrodes placed parallel to or across the length of the intestine (longitudinal and transverse electrodes, respectively). In preparations of circular muscle with the myenteric plexus attached, the mean amplitude of i.j.p.s recorded 9 mm lateral to longitudinal electrodes was about 70% of that seen at 1 mm; however, in the presence of hexamethonium (400 microM) the amplitude fell more rapidly to about 40% at 9 mm. The decline was even steeper in preparations of circular muscle from which the myenteric plexus had been removed, with the amplitude falling to 10% at 9 mm. I.j.p.s were detected up to 30 mm anal to stimuli applied with transverse electrodes in the presence of hexamethonium, but the decline was more rapid on the oral side, with i.j.p.s being detected only up to 12 mm oral to the stimulus. Nerves that travel through or originate in the myenteric plexus were severed or removed in operations performed 2-7 days before tissue was taken. 2-3 days after removal of a circumferential strip of myenteric plexus, i.j.p.s could not be recorded from the underlying circular muscle. I.j.p.s evoked by longitudinal electrodes were recorded in an area between two circumferential cuts through the myenteric plexus, 1.5-8 mm apart, 3-7 days after an operation. In this region, the i.j.p.s were significantly smaller than normal although amplitudes of up to 95% of control were measured. The consequences of single circumferential cuts through the myenteric plexus were examined 3 and 7 days after operation. Longitudinal electrodes were used to stimulate surviving fibres. Small i.j.p.s were recorded on the anal edge of the lesion; the amplitude recovered to 56% of normal in the first 2 mm on the anal side and the amplitude slowly returned to normal at 20 mm anal. On the oral side there was slight reduction in amplitude at 0.5 and 1 mm, but at greater distances amplitudes were normal. It is concluded that the simplest explanation of these results is that two populations of i.j.p.-producing neurones have their cell bodies in the myenteric plexus. Many axons supply the circular muscle close to or just anal to their cell bodies, and others run for various distances up to 30 mm in the anal direction.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed2004

[Altered colonic transit in TNBS-induced experimental colitis in guinea pig and distribution of nitric oxide synthase in the colonic wall].

BACKGROUND/AIMS: Inflammation-induced alterations in smooth muscle contractility may be due to the effects on smooth muscle itself, neurotransmitters or enteric nerves. In dextran sulfate sodium-induced colitic rat, the delay in colonic transit was caused by decreased activity and production of neuronal nitric oxide synthase (nNOS) in the myenteric plexus of the distal colon. The aim of this study was to investigate the relationship between the delay in colonic transit and the distribution of inducible NOS (iNOS) and nNOS immunoreactive cells in the myenteric plexus of trinitrobenzene sulfonic acid (TNBS)-induced colitic guinea pig. METHODS: Sacrificed and their colonic tissues of forty-five TNBS-induced colitic guinea pigs were used to measure the colonic transit, and analyzed by immunohistochemistry. RESULTS: Colonic transit was delayed significantly at 3, 7 and 14 days after administration of TNBS. In control, nNOS immunoreactivity was present in the mucosa, submucosa, lamina propria, and ganglion cells of the myenteric plexus, while after TNBS treatment, reduced nNOS cells were found. However, the number of nNOS ganglion cells in the myenteric plexus was similar to those seen in controls. After administration of TNBS, iNOS immunoreactivity was increased in the mucosa and submucosa, but the number of iNOS positive ganglion cells in the myenteric plexus was not changed compared to control. CONCLUSIONS: It is suggested that in TNBS-induced guinea pig colitis, delayed colonic transit is not associated with the expression of nNOS nor iNOS in the myenteric plexus.

Animals↗