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PubMed1998

Extrinsic neural control of nitric oxide synthase expression in the myenteric plexus of rat jejunum.

1. The role of extrinsic innervation in the expression of nitric oxide synthase (NOS) in the myenteric plexus remains unknown. In this study, we investigated the effect of extrinsic denervation on NOS expression in rat jejunum. 2. NG-nitro-L-arginine methyl ester (L-NAME)-sensitive non-adrenergic, non-cholinergic (NANC) relaxations induced by transmural nerve stimulation were significantly increased in muscle strips obtained from rats treated with splanchnic ganglionectomy or 6-hydroxydopamine (6-OH-dopamine). Truncal vagotomy or treatment of the coeliac ganglia with capsaicin did not significantly affect NANC relaxations. 3. The number of NOS-immunopositive cells in the myenteric plexus was significantly increased in tissues obtained from rats treated with splanchnic ganglionectomy or 6-OH-dopamine. 4. Western blot analysis and Northern blot analysis showed a significant increase in the density of the immunoreactive NOS band and the NOS mRNA band, respectively, of the tissues obtained from rats treated with splanchnic ganglionectomy or 6-OH-dopamine. 5. Truncal vagotomy or treatment of the coeliac ganglia with capsaicin did not significantly affect the density of NOS band or NOS mRNA band. 6. It is concluded that neuronal NOS expression in the myenteric plexus is independent of vagus nerve and is negatively regulated by the splanchnic nerves in the rat small intestine.

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PubMed1997

Impaired expression of nitric oxide synthase in the gastric myenteric plexus of spontaneously diabetic rats.

BACKGROUND & AIMS: The mechanism responsible for defective gastric accommodation in diabetes is unknown. The aim of this study was to investigate if this abnormality is due to a defective nitric oxide pathway secondary to impaired nitric oxide synthase (NOS) expression in the gastric myenteric plexus. METHODS: To test this hypothesis, we studied nonadrenergic, noncholinergic (NANC) relaxation, NOS activity, NADPH diaphorase histochemistry, NOS immunohistochemistry, NOS immunoblotting, and NOS messenger RNA expression in the gastric myenteric plexus of spontaneously diabetic biobreeding/Worcester (BB/W) rats. Age-matched nondiabetic Wistar rats were used as controls. RESULTS: Gastric neuromuscular preparations from control rats showed a frequency-dependent NANC relaxation in response to transmural stimulation. This relaxation was markedly antagonized by N(G)-nitro-L-arginine-methyl ester, indicating mediation by the neuronal release of NO. The NANC relaxation in gastric muscle preparations obtained from diabetic BB/W rats was significantly impaired. The number of NOS-immunoreactive cells in the gastric myenteric plexus and the NOS activity were significantly reduced in diabetic BB/W rats, suggesting that NOS synthesis is impaired in diabetes. Northern blot analysis showed that the density of NOS messenger RNA bands at 9.5 kilobases was significantly reduced in the gastric tissues of diabetic BB/W rats. CONCLUSIONS: These results indicate that gastric relaxation in diabetics is hampered mainly by impaired NOS expression in the gastric myenteric plexus.

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PubMed1990

Stimulation of acetylcholine release in myenteric plexus by calcitonin gene-related peptide.

The effects of calcitonin gene-related peptide (CGRP) on acetylcholine (ACh) release from myenteric plexus neurons in primary culture were investigated. CGRP (10(-12) to 10(-6) M) produced a dose-dependent increase in [3H]ACh release. The ACh release caused by CGRP was significantly inhibited (74 +/- 24%) by preincubation with dideoxyadenosine but was increased more than threefold by preincubation with theophylline. Incubation of myenteric plexus neurons with CGRP (10(-8) M) in the presence of diltiazem (10(-5) M) or in a calcium-free medium markedly reduced [3H]ACh release. CGRP potentiated [3H]ACh release stimulated by potassium or substance P but not by cholecystokinin octapeptide or forskolin. The results demonstrate that CGRP cause release of ACh from guinea pig myenteric plexus neurons and suggest that the peptide acts through an adenosine 3',5'-cyclic monophosphate-dependent mechanism that involves neuronal calcium channels.

Acetylcholine↗

PubMed1998

A neurochemical characterisation of the golden hamster myenteric plexus.

The neurochemical composition of nerve fibres and cell bodies in the myenteric plexus of the proventriculus, stomach and small and large intestines of the golden hamster was investigated by using immunohistochemical and histochemical techniques. In addition, the procedures for localising nitric-oxide-utilising neurones by histochemical (NADPH-diaphorase) and immunohistochemical (nitric oxide synthase) methods were compared. The co-localisation of vasoactive intestinal polypeptide and nitric oxide synthase in the myenteric plexus of all regions of the gut was also assessed. The results demonstrated the presence of nerve fibres and nerve cell bodies immunoreactive to protein gene product, vasoactive intestinal polypeptide, substance P, calcitonin gene-related peptide, tyrosine hydroxylase, 5-hydroxytryptamine and nitric oxide synthase in all regions of the gastrointestinal tract examined. The pattern of distribution of immunoreactive nerve fibres and nerve cell bodies containing the above markers was found to vary in different regions of the gut. Myenteric neurones and nerve fibres containing immunoreactivity to nitric oxide synthase and NADPH-diaphorase reactivity, however, were shown to have an identical distribution throughout the gut. In contrast to some studies on the guinea-pig and rat, the co-existence of vasoactive intestinal polypeptide and nitric oxide synthase was seen in only a small population of myenteric neurones.

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PubMed1991

Chronic treatment of guinea pigs with lithium chloride: effects on myenteric plexus preparations and on cyclic AMP levels.

We studied the effects of lithium chloride, given i.p. in doses of 0.05, 1, 2, 4 and 8 mEq/kg twice daily for 14 days, on preparations of guinea pig myenteric plexus. The effects of lithium added to isolated myenteric plexus preparations derived from chronically treated animals showed that relatively low lithium concentrations produced a statistically significant decrease in the force of contraction, this effect being concentration-dependent. 3-Isobutyl-1-methylxanthine (IBMX) induced a statistically significant inhibition, between 30 and 50%, of the lithium effects. cAMP levels in animals treated chronically with lithium were studied, using an isotopic displacement technique. Our results show that only the highest dose of lithium (8 mEq/kg per day) significantly decreased basal levels of cAMP. In the presence of IBMX, low doses of lithium (1 mEq/kg per day) induced a very significant decrease in cAMP levels, but the inhibition remained constant, approximately 30-35%, at doses from 2 mEq/kg per day. In guinea pig myenteric plexus preparations from acutely treated animals, our results show a direct relationship between lithium concentration and inhibition of the cAMP accumulation induced by IBMX.

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PubMed1994

Myenteric plexus explants promote neurite elongation and survival of striatal neurons in vitro.

Dissociated striatal neurons exhibited increased neurite outgrowth when co-cultured with myenteric plexus explants. Enriched enteric neurons or enriched enteric glia produced a less marked response; non-ganglionic cells had no effect. Increases in striatal neuron and glial cell numbers were seen in all co-cultures. Tetrodotoxin abolished the neuritogenic response of myenteric plexus explants but did not affect increases in cell numbers. These observations suggest that spontaneous neuronal activity within the myenteric plexus is involved in the release of a neuritogenic factor(s), possibly from glial cells, and that this is distinct from the factor(s) affecting striatal cell numbers.

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PubMed1993

Effect of lanthanum ions on the release of acetylcholine induced by tityustoxin, K+ and ouabain from myenteric plexus and brain cortical slices.

Exposure of myenteric plexus longitudinal muscles to 2 mM LaCl3 increased the rate of spontaneous [3H]-ACh release. In brain cortical slices La3+ did not affect the spontaneous release of ACh. The release of ACh induced by tityustoxin, ouabain or K+ 50 mM in brain cortex and myenteric longitudinal muscles slices was inhibited by La3+ treatment. It is suggested that tityustoxin, ouabain and K+ release ACh from the same pool that is inhibited by La3+ pretreatment.

Acetylcholine↗

PubMed1999

Morphological changes of the myenteric plexus during early postnatal development of the rat.

The enteric nervous system needs to adapt itself constantly to the postnatal changes of the developing gut. The aim of this study was to examine the morphological changes between the distal and proximal segments of the gastrointestinal (GI) tract during the first two postnatal weeks. Myenteric plexus from the duodenum, proximal and distal colon of 1-, 7- and 14-day-old rat pups was dissected and examined under the scanning electron microscope. Wholemounts from the same regions and postnatal stages were stained with cuprolinic blue. Neuronal numbers per ganglionic area were counted and neuronal sizes were measured. Furthermore, segments of the above-mentioned areas were embedded in resin and semithin sections were cut. The thickness of the circular and longitudinal muscle layers was measured. The morphology of the myenteric plexus depends on localization as well as on the age of the animal. While in younger animals the myenteric plexus is usually densely packed, the network expands with increasing age. Similarly, the thickness of the circular and the longitudinal muscle layers increases. Nerve cell numbers per ganglionic area increase from duodenum to distal colon and decrease from the 1-day (P1) to the 14-day-old (P14) animal. The longest diameters and the area of the nerve cells decrease from duodenum to distal colon and increase with age of the animal. The intensity of the cuprolinic blue staining varies also according to age and segment of the gut. During the first two postnatal weeks the three-dimensional architecture of the myenteric plexus as well as the size and densities of the enteric neurons change according to the increasing gut length and the thickness of the muscle layer. The differences between duodenum and colon might reflect the different physiological properties of the proximal and distal gut as well as a varying grade of maturity, which is also supported by a variation in the cuprolinic blue staining intensity.

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PubMed2001

Distribution and chemical coding of orphanin FQ/nociceptin-immunoreactive neurons in the myenteric plexus of guinea pig intestines and sphincter of Oddi.

Longitudinal muscle-myenteric plexus preparations of guinea pig intestines and sphincter of Oddi (SO) were immunostained for orphanin FQ/nociceptin. Orphanin FQ-immunoreactive (OFQ-IR) neurons and nerve fibers were relatively abundant in the SO, duodenum, ileum, cecum, and distal colon, with fewer neurons and nerve fibers observed in the proximal colon. Double staining with antibodies directed against the neuron-specific RNA binding protein Hu revealed that while the numbers of OFQ-IR neurons per ganglion decreased along the gut tube, similar proportions (7-9%) of neurons in these regions were OFQ-IR, whereas <1% of the neurons in the proximal colon were OFQ positive. In the ileum, where 8% of the myenteric neurons were OFQ-IR, all OFQ-IR neurons expressed choline acetyltransferase. In addition, multiple-label immunohistochemistry demonstrated that 58% of the OFQ-IR neurons were calretinin-IR, 52% were substance P-IR, and 28% were enkephalin-IR. Nitric oxide synthase immunoreactivity was observed in about 5% of OFQ-IR neurons, or 0.4% of the total population, and a similar proportion of the OFQ-IR neurons was positive for vasoactive intestinal peptide. No OFQ-IR neurons were immunoreactive for calbindin, somatostatin, or serotonin. These results, combined with previous studies of chemical coding and projection patterns in the guinea pig myenteric plexus, indicate that OFQ-IR is expressed preferentially in excitatory motor neurons projecting to the longitudinal and circular muscle layers, as well as a small subgroup of descending interneurons. Because OFQ is expressed by excitatory motor neurons, and because this peptide inhibits excitatory neurotransmission in the guinea pig ileum, it is likely that OFQ acts through a feedback autoinhibitory mechanism.

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PubMed2005

Choline acetyltransferase and inducible nitric oxide synthase are increased in myenteric plexus of diabetic guinea pig.

Alterations in enzymes in myenteric neurons from ileum were investigated in guinea pigs treated with either the pancreatic beta cell toxin streptozotocin or vehicle. After 5-6 weeks, expressions of choline acetyltransferase, neuronal nitric oxide synthase and inducible nitric oxide synthase were determined in longitudinal and myenteric plexus preparations using indirect immunohistochemistry. In ileum from streptozotocin-treated animals, the density of choline acetyltransferase-immunoreactive nerve fibers within the tertiary plexus and the percent total myenteric neurons expressing inducible nitric oxide synthase were increased, but the percent total myenteric neurons expressing neuronal nitric oxide synthase was not changed. Diabetes resulted in selective alterations in myenteric neurons including an increased density of cholinergic tertiary fibers and percentage of neurons expressing the inducible isoform of nitric oxide synthase. These adaptive changes by myenteric neurons to diabetes may contribute to gastrointestinal dysfunctions associated with diabetes.

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PubMed1993

Bombesin-stimulated acetylcholine release from myenteric plexus neurons.

The ability of bombesin to stimulate acetylcholine release from guinea pig myenteric plexus neurons was studied using a primary neuronal culture system. Bombesin caused dose-dependent increases in [3H]-acetylcholine (ACh) release from guinea pig myenteric plexus neurons. ACh release in response to 0.5 mM bombesin (160 +/- 12% of control) was blocked by exposure to a calcium-free medium (116 +/- 13%) by nifedipine (101 +/- 11%) and by omega conotoxin (107 +/- 10%). Bombesin-stimulated ACh release was inhibited the protein kinase C inhibitor, H7, but was not affected by inhibitors of the cAMP signaling pathway. Interactions with inhibitory neuropeptides was implied by sensitivity of bombesin-stimulated ACh release to neuropeptide Y and galanin. The findings suggest that bombesin activation of protein kinase C in myenteric neurons results in increased acetylcholine release.

Acetylcholine↗

PubMed1987

[Interaction of opioid peptides and the dopaminergic system in the myenteric plexus of the guniea pig ileum].

The effects of treatment with dopamine agonists and 6-hydroxydopamine on the release of opioid peptides from the myenteric plexus of guinea-pig ileum were examined. Apomorphine or bromocriptine treatment at doses that act on dopamine autoreceptors to inhibit dopamine release resulted in a significant elevation of the release of opioid peptides. 6-hydroxydopamine treatment, which produces a lesion of catecholaminergic nerve terminals also resulted in an increase in opioid peptide release. These findings indicate that interruption of dopaminergic transmission in the myenteric plexus produces an increase in the release of opioid peptides and suggest an inhibitory modulation of opioid peptidergic neurons by dopamine systems in the myenteric plexus of the guinea-pig ileum.

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PubMed1988

Intrinsic and extrinsic innervation of the amphibians esophagic myenteric plexuses.

The innervation of Rana ridibunda esophagus myenteric plexuses has been studied by the following methods: demonstration of cholinesterase activity; FIF method for catecholamines; immunohistochemistry for VIP, SP and SOM, and conventional electron microscopy. The cholinergic innervation is important in the esophagus wall where, in addition to the well known extrinsic component, there is a rich intrinsic plexus with cells and fibres widely distributed. The esophagus, together with the intestine, are the Rana gut portions where the adrenergic component is more broadly expressed. The adrenergic innervation seems to be almost entirely of extrinsic origin. We have shown that, for the tested peptides, there is an intrinsic innervation represented by VIP, SP and SOM like plexuses. We do not discard nonetheless an extrinsic component. The ultrastructure reveals the morphological characteristics of the enteric neurons as well as the fine inter-relationships between the nervous elements and the functional components of the esophagic wall.

Animals↗

PubMed1985

Shunt fascicles in the gastric myenteric plexus in five species.

Thick nerve bundles, called shunt fascicles, lie in the myenteric plexus of the stomach in guinea pig, rabbit, cat, opossum, and cynomolgus monkey. They enter the stomach at the cardia, either as extensions of the esophageal myenteric plexus or of vagal branches to the caudal esophagus, and radiate toward the greater curvature. They bypass ganglia in the orad part of the stomach but give off branches to ganglia in more caudad parts. They are more abundant in the gastric fundus and body than in the antrum; they are infrequent along the greater curvature of the antrum. About 4% of the fibers they contain are myelinated. Arterioles and venules follow shunt fascicles and give rise to perifascicular capillary networks. Shunt fascicles are prominent in the cat, opossum, and monkey; they are short, thin, and sparse in the rabbit and guinea pig. They do not appear to be extensions of the direct vagal branches to the stomach but may be special nerve pathways from the esophagus to parts of the stomach.

Animals↗

PubMed1987

Peripheral nerve fibres regenerate through myenteric plexus.

The ability of myenteric glia and neurons to support peripheral nerve regeneration was tested by grafting pieces of muscularis externa 5 mm long from the distal colon of inbred CBA mice adjacent to the proximal stump of cut common peroneal nerves. By two weeks after operation many axons had invaded the plexus and after 3 weeks regeneration common peroneal nerve fibres could be identified in all parts of the plexus throughout the grafts. Some axonal profiles within the plexus appeared to be in the early stages of myelination by enteric glia. Axons surrounded by compact myelin were found at the periphery of ganglia, but the cells involved resembled Schwann cells and could not be positively identified as enteric glia. Profiles similar to those of regenerating axons were only very rarely seen in control experiments in which grafts were placed adjacent to intact common peroneal nerves. It is suggested that the cellular elements of the myenteric plexus can support peripheral nerve regeneration.

Animals↗

PubMed2006

Endogenous cholecystokinin reduces food intake and increases Fos-like immunoreactivity in the dorsal vagal complex but not in the myenteric plexus by CCK1 receptor in the adult rat.

We hypothesized that endogenous CCK reduces food intake by activating the dorsal vagal complex (DVC) and the myenteric neurons of the gut. To test this hypothesis, adult rats were given camostat mesilate; a nonnutrient releaser of endogenous CCK, by orogastric gavage, and Fos-like immunoreactivity (Fos-LI) was quantified in the DVC and the myenteric plexus. The results for endogenous CCK were compared with those for exogenous CCK-8. Exogenous CCK-8 reduced food intake and stimulated Fos-LI in the DVC and in myenteric neurons of the duodenum and jejunum. In comparison, endogenous CCK reduced food intake and increased DVC Fos-LI but did not increase Fos-LI in the myenteric plexus. Similar to CCK-8, devazepide, a specific CCK(1) receptor antagonist, and not L365,260, a specific CCK(2) receptor antagonist, attenuated the reduction of food intake by camostat. In addition, Fos-LI in the DVC in response to both exogenous CCK-8 and camostat administration was significantly attenuated by vagotomy, as well as by blocking CCK(1) receptors. These results demonstrate for the first time that reduction of food intake in adult rats by endogenous CCK released by a nonnutrient mechanism requires CCK(1) receptors, the vagus nerve, and activation of the DVC, but not the myenteric plexus.

Animals↗

PubMed1986

Direct analysis of the release of methionine-enkephalin from guinea pig myenteric plexus: modulation by endogenous opioids and exogenous morphine.

The in vitro release of methionine-enkephalin (met-enkephalin) from two longitudinal muscle myenteric plexus strips from guinea pig ileum has been obtained during continuous superfusion and quantitated directly using a radioimmunoassay specific for this opioid peptide. Electrical stimulation (5-80 Hz) produced a significant increase in the rate of release of met-enkephalin the magnitude of which was not dependent on the frequency of stimulation. Analysis of the release of met-enkephalin per pulse as a function of the frequency of stimulation indicated that the release of this opioid peptide from the myenteric plexus is inversely proportional to the frequency of stimulation. Electrically evoked release (40 Hz) of met-enkephalin was reduced by greater than 80% by substituting CoCl2 for CaCl2 or by pretreatment with tetrodotoxin (1 microgram/ml for 15 min). Evoked release was also reduced substantially by pretreatment with morphine (1 microM, 1.5 min). Alternatively, pretreatment of naive longitudinal muscle myenteric plexus strips with the opiate antagonist (-)-naloxone caused a significant increase in the rate of met-enkephalin release in the absence of electrical stimulation. In contrast, (+)-naloxone was devoid of any activity. These data, in combination with indirect pharmacological experiments, strongly indicate that met-enkephalin functions as a neurotransmitter in the enteric nervous system. Moreover, the activity of neurons that transmit via met-enkephalin appears to be under opioid regulation.

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PubMed1983

Actions of Ca2+ antagonists on the guinea-pig ileal myenteric plexus preparation.

The guinea-pig ileal myenteric plexus preparation has been used to compare the actions of three Ca2+ channel antagonists, D 600 (methoxyverapamil), nicardipine and diltiazem, on smooth muscle contractions and acetylcholine release in response to electrical stimulation. Acetylcholine release was not affected by these agents at concentrations of 10(-6)-10(-5)M. In confirmation of previous work, however, the smooth muscle contractile responses were effectively inhibited at these concentrations. Quercetin, a non-Ca2+ channel antagonist, was approximately equieffective in blocking both acetylcholine release and smooth muscle contractions. These data suggest that differences may exist in the antagonist sensitivity of voltage-dependent Ca2+ channels.

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