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PubMed2001

Quantitative study of the myenteric plexus of the stomach of rats with streptozotocin-induced diabetes.

The purpose of the present study was to investigate the morphological and quantitative alterations of the myenteric plexus neurons of the stomach of rats with streptozotocin-induced chronic diabetes and compare them to those of non-diabetic animals. Samples from the body of the stomach were used for whole-mount preparations stained with NADH-diaphorase and for histological sections stained with hematoxylin-eosin. It was observed that diabetes cause a significant decrease on the number of neurons.

Animals↗

PubMed1985

Neurochemical evidence for the release of acetylcholine from the guinea-pig ileum myenteric plexus by capsaicin.

Superfusion of the sensory stimulant drug capsaicin (3.3 microM) released [3H]acetylcholine from isolated myenteric plexus-longitudinal muscle strips of guinea-pig ileum, preincubated with [3H]choline. This effect was prevented by tetrodotoxin. There was a fast tachyphylaxis to the effect of capsaicin. It is suggested that capsaicin-sensitive nerve endings capable of activating intrinsic cholinergic neurones are situated in the myenteric plexus of the guinea-pig ileum.

Acetylcholine↗

PubMed1986

The distribution of GABA-transaminase-dehydrogenase activity in the myenteric plexus of rat small intestine: a histochemical analysis.

The presence and distribution of gamma-aminobutyric acid (GABA) degradative enzyme (GABA transaminase-succinic semialdehyde dehydrogenase) activity in the rat myenteric plexus was determined histochemically using laminar preparations of the small intestine. Blue-diformazan staining resulting from reduction of the tetrazolium salt, Nitro-BT, during GABA catabolism was present in a scattered population of ileal and jejunal myenteric ganglion cells, including those resembling multipolar type II and unipolar nerve cells. Such staining was almost completely prevented under conditions of GABA-T inhibition. These results indicate that GABA is enzymically degraded at specific sites in the rat enteric nervous system where it is proposed to have a neurotransmitter function.

4-Aminobutyrate Transaminase↗

PubMed1982

Cholinergic modulation of the release of [3H]acetylcholine from synaptosomes of the myenteric plexus.

The purpose of these experiments was to determine if cholinergic agents affected the release of acetylcholine (ACh) from a synaptosomal preparation of the guinea pig ileum myenteric plexus. The synaptosomal preparation was first incubated with the precursor [3H]choline; subsequently, release of the stored [3H]ACh was measured. The release was decreased by oxotremorine or exogenous ACh plus hexamethonium and increased by exogenous ACh plus evoked release that was inhibited by nicotinic antagonists or muscarinic agonists. Release was stimulated half-maximally by approximately 2 microM- and maximally by 10 microM-DMPP. Either in the absence of calcium or at 0 degrees C, DMPP was without effect. The effect of 10 microM-DMPP was brief, a significant stimulation occurring only within the first 2 min at 37 degrees C. Tetrodotoxin also inhibited excitation by DMPP but not completely. Thus, the release of [3H]ACh appears to be presynaptically modulated, negatively by muscarinic agonists and positively by nicotinic agonists.

Acetylcholine↗

PubMed1988

Agonists, antagonists and modulators of excitatory amino acid receptors in the guinea-pig myenteric plexus.

1. The receptors for glutamic acid (L-Glu) present in the guinea-pig myenteric plexus-ileal longitudinal muscle preparation have been studied by measuring the muscle contraction induced by numerous putative endogenous agonists acting at these receptors. Furthermore, the actions of different concentrations of antagonists, glycine, Mg2+ and Ca2+ on the ileal contractions induced by L-Glu have been evaluated. 2. The EC50 values of the most common putative endogenous agonists of these receptors were: L-Glu 1.9 X 10(-5) M; L-aspartate 8 X 10(-5) M; quinolinate 5 X 10(-4) M; L-homocysteate 1.4 X 10(-4) M; the dipeptide aspartyl-glutamate 8 X 10(-5) M, while N-acetyl-aspartyl-glutamate was inactive. Among the molecules used to classify excitatory amino acid receptors, N-methyl-D-aspartate (NMDA) was the most potent (EC50 5 X 10(-4) M). Kainic and quisqualic acids were almost completely inactive. 3. The responses to L-Glu were competitively antagonized by 2-amino-5-phosphonovaleric acid. They were, also, prevented by hyoscine (10(-7) M) and by tetrodotoxin (3 X 10(-7) M), suggesting that the L-Glu-induced ileal contraction was in some way dependent upon an action on the myenteric cholinergic neurones. Kynurenic acid was a non-competitive antagonist, gamma-D-glutamyl-taurine (10(-4) M) and aminophosphonobutyric acid (10(-4) M) did not modify the L-Glu-induced contractions. 4. Glycine (10(-5) M) significantly potentiated the effects of glutamate especially when the ionic composition of the superfusion medium contained concentrations of Ca2+ in the range of 0.6-1.2 mM. Strychnine 3 X 10(-5) M did not modify the actions of glycine. 5. The data presented here confirm the presence of NMDA receptors in the guinea-pig myenteric plexus, and show that these receptors, similar to those present in primary neuronal cultures may be modulated by glycine.

Animals↗

PubMed1998

Relationship between muscarinic autoinhibition and the inhibitory effect of morphine on acetylcholine release from myenteric plexus of guinea pig ileum.

The relationship between muscarinic autoinhibition and the inhibitory effect of morphine on acetylcholine (ACh) release was investigated in a longitudinal muscle with myenteric plexus (LMMP) preparation of guinea pig ileum. Morphine (10 microM) inhibited spontaneous and evoked ACh release by electrical field stimulation (EFS) at 1 Hz but not at 10 Hz. Atropine (1 microM) did not affect the resting ACh release, but it significantly increased EFS-evoked release, suggesting activation of muscarinic autoreceptors by ACh released during EFS. Only when the autoinhibition was weakened by atropine, morphine exhibited an inhibitory effect on the EFS-evoked release at 10 Hz. Bethanechol (300 microM) inhibited the EFS-evoked release at 1 Hz but not 10 Hz, suggesting that muscarinic autoreceptors are partially or almost fully activated at 1 or 10 Hz stimulation, respectively. After bethanechol treatment, morphine did not exhibit its inhibitory effect on the EFS-evoked release at 1 Hz. Naloxone (1 microM) increased spontaneous and EFS-evoked ACh release at 1 Hz but not at 10 Hz. Following treatment with atropine, naloxone also increased ACh release at 10-Hz stimulation. These results suggest that morphine and an endogenous opioid inhibit ACh release from LMMP preparations when muscarinic autoinhibition mechanism does not fully work. This inhibitory effect of morphine is discussed in relation to the calcium sensitivity of the preparations in ACh release.

Acetylcholine↗

PubMed1998

Evidence that cannabinoid-induced inhibition of electrically evoked contractions of the myenteric plexus--longitudinal muscle preparation of guinea-pig small intestine can be modulated by Ca2+ and cAMP.

Cannabinoid receptor agonists inhibit electrically evoked isometric contractions of the myenteric plexus--longitudinal muscle preparation of the guinea-pig small intestine (MPLM), probably by reducing release of acetylcholine (ACh) through the activation of prejunctional CB1 receptors. As CB1 receptors are thought to be negatively coupled through Gi/o proteins to both N-type Ca2+ channels and adenylate cyclase, we have now further investigated the involvement of CB1 receptors by monitoring the effects of forskolin, 8-bromo-cAMP, 3-isobutyl-1-methylxanthine (IBMX), and extracellular Ca2+ on the ability of the cannabinoid agonist, (+)-WIN 55212 to inhibit electrically evoked contractions of the MPLM (0.1 Hz, 0.5 ms, and 110% maximal voltage). Some experiments were performed with normorphine instead of (+)-WIN 55212. At 10(-7) M, forskolin, 8-bromo-cAMP, and IBMX were found to reduce significantly the maximum inhibitory response to (+)-WIN 55212 by 49.4, 48.4, and 40.2%, respectively, without affecting control contractions or responses to exogenous ACh. Low external Ca2+ (0.64 mM) significantly increased the maximum response to (+)-WIN 55212 and shifted the curve slightly leftwards, whereas high external Ca2+ (5.08 mM) reduced the maximum response by 27.2%. The concentration-response curve to normorphine, which also reduces evoked contractions of this preparation as a result of a presynaptic inhibition of ACh release via opioid mu receptors, was affected similarly. These results support the hypothesis that cannabinoid-induced inhibition in the MPLM is mediated by CB1 receptors.

1-Methyl-3-isobutylxanthine↗

PubMed1993

Serotonin-induced increase in cAMP in ganglia isolated from the myenteric plexus of the guinea pig small intestine: mediation by a novel 5-HT receptor.

Serotonin (5-HT) is a mediator (through 5-HT1P receptors) of slow EPSPs in myenteric ganglia of the small intestine. The effect of 5-HT can be mimicked by elevating cAMP; therefore, we tested the hypothesis that the slow EPSP-like response to 5-HT is cAMP-mediated. Guinea pig gut was enzymatically dissociated; myenteric ganglia remained intact and were collected by filtration. Neurons in the isolated ganglia retained their ability to manifest the slow EPSP-like response to 5-HT. Exposure to 5-HT raised the ganglionic level of cAMP (ED50 0.3 microM). This effect was not antagonized by the 5-HT1P antagonist, N-acetyl-5-hydroxytryptophyl-5-hydroxytryptophan amide (100.0 microM), or mimicked by the 5-HT1P agonist, 5-hydroxyindalpine (10.0 microM). Increases in cAMP were also evoked by the 5-HT1 agonist, 5-carboxyamidotryptamine (10.0 microM), the 5-HT2 agonist, (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI; 1.0-10.0 microM), and by the 5-HT4 agonists, renzapride (1.0-10.0 microM) and 5-methoxytryptamine (1.0-10.0 microM); however, neither the 5-HT1/5-HT2 antagonists, spiperone, methysergide, and methiothepin, nor the 5-HT4 antagonist, tropisetron (ICS 205-930; 10.0 microM), were able to inhibit the rise in cAMP evoked by these compounds or by 5-HT (0.1-10.0 microM). The 5-HT-evoked elevation of cAMP was antagonized by ketanserin (10.0 microM), which also blocked the effects of 5-methoxytryptamine and DOI, but not those of renzapride. The effective concentration of DOI, however, was higher than that needed for activation of 5-HT2 receptors, and Northern analysis using a cDNA probe encoding the rat 5-HT2 receptor failed to reveal the presence of 5-HT2 mRNA in myenteric ganglia, although it hybridizes with mRNA of the right size in the guinea pig brain. Compounds that failed to change levels of cAMP or to antagonize the action of 5-HT included 8-hydroxy-di-n-propylamino tetralin, R58639, R88226, and sumatriptan. It is concluded that the receptor responsible for the 5-HT-induced rise in cAMP in ganglia isolated from the guinea pig myenteric plexus is not a known subtype of 5-HT receptor. Since the pharmacology of this novel receptor is different from that of the slow EPSP-like response to 5-HT, the receptor probably does not mediate the slow EPSP.

Acetylcholinesterase↗

PubMed1991

Histamine H3 receptors regulate acetylcholine release from the guinea pig ileum myenteric plexus.

The effect of selective histamine H3-receptor agonists and antagonists on the acetylcholine release from peripheral nerves was evaluated in the guinea pig longitudinal muscle-myenteric plexus preparations, preloaded with (3H)choline. In the presence of H1 and H2 blockade, histamine (10(-7)-10(-4) M) and (R)-alpha-methylhistamine (10(-8)-10(-6) M) inhibited the electrically-evoked acetylcholine release, being (R)-alpha-methylhistamine more active than histamine, but behaving as a partial agonist. The effect of histamine was completely reversed by selective H3-blocking drugs, thioperamide and impromidine, while only submaximal doses of (R)-alpha-methylhistamine were antagonized. Furthermore, thioperamide and impromidine enhanced the electrically-evoked acetylcholine release. On the contrary, the new H3-blocker, HST-7, was found substantially ineffective, both as histamine antagonist and as acetylcholine overflow enhancer. These data suggest that histamine exerts an inhibitory control on the acetylcholine release from intestinal cholinergic nerves through the activation of H3 receptors.

Acetylcholine↗

PubMed1993

Vasoactive intestinal peptide release and L-citrulline production from isolated ganglia of the myenteric plexus: evidence for regulation of vasoactive intestinal peptide release by nitric oxide.

Vasoactive intestinal peptide release and L-[3H]citrulline production were examined in ganglia isolated from the myenteric plexus of guinea-pig intestine. The nicotinic agonist, 1,1-dimethyl-4-phenylpiperizinium stimulated vasoactive intestinal peptide release and L-[3H]citrulline production; the latter was considered an index of nitric oxide production. Both vasoactive intestinal peptide release and L-[3H]citrulline production were abolished by tetrodotoxin, hexamethonium, and the nitric oxide synthase inhibitor, NG-nitro-L-arginine. Inhibition of vasoactive intestinal peptide release by NG-nitro-L-arginine was reversed by L-arginine but not by D-arginine. Exogenous nitric oxide stimulated vasoactive intestinal peptide release whereas exogenous vasoactive intestinal peptide had no effect on L-[3H]citrulline production. The pattern of stimulation by nitric oxide and inhibition by NG-nitro-L-arginine implied that vasoactive intestinal peptide release is facilitated by and may be dependent on nitric oxide production. Consistent with this notion, vasoactive intestinal peptide release in response to either 1,1-dimethyl-4-phenylpiperizinium or nitric oxide was abolished by KT 5823, an inhibitor of cyclic GMP-dependent protein kinase activity and by LY83583, an inhibitor of soluble guanylate cyclase activity. The study provides the first direct evidence of nitric oxide production from enteric ganglia.

Alkaloids↗

PubMed1991

Effect of atrial natriuretic factor and 8-bromo cyclic guanosine 3':5'-monophosphate on [3H]acetylcholine outflow from myenteric-plexus longitudinal muscle of the guinea pig.

We report that atrial natriuretic factor (ANF) inhibits electrically induced cholinergic twitches of longitudinal muscle in whole intestinal segments and myenteric-plexus longitudinal muscle (MPLM) strips from the guinea pig ileum. To elucidate the possible presynaptic mechanism of ANF's action, we studied spontaneous and stimulation-evoked radiolabeled acetylcholine (ACh) outflow from MPLM after incubation with [3H]choline. We developed a method of mounting and treating MPLM preparations, which allowed us, at the same time, to record isometric contractions and to determine [3H]ACh outflow upon electrical stimulation by a train of three pulses. ANF (5 x 10(-8) M), norepinephrine (2 x 10(-7) M) and 8-bromoguanosine 3':5'-cyclic monophosphate (10(-3) M) in nearly equieffective concentrations caused a similar inhibition of cholinergic twitches. However, ANF had no effect on [3H]ACh outflow, whereas norepinephrine was found to suppress [3H]ACh outflow and 8-bromoguanosine 3':5'-cGMP to enhanced [3H]ACh outflow. ANF (5 x 10(-8) M) caused a 7.0-fold increase of cGMP over control values, predominantly in muscle layers, whereas Escherichia coli heat-stable toxin (12.5 U/ml) elicited a 35-fold increment of cGMP in the extramuscular layer. Thus, ANF is able to elevate cGMP in intestinal smooth muscle and to inhibit cholinergic contractions of MPLM. This inhibition is mimicked by exogenous cGMP and by endogenously generated cyclic nucleotides. We suggest that the depressive action of ANF on cholinergic contractions of MPLM is mediated via its postsynaptic impact implicating elevation of cGMP in smooth muscle.

1-Methyl-3-isobutylxanthine↗

PubMed1978

Effect of lithium chloride on electrically stimulated guinea-pig longitudinal muscle-myenteric plexus.

Lithium chloride, in the concentration range of 10(-4)M to 10(-2)M, increases the height of electrically induced contractions of guinea-pig longitudinal muscle-myenteric plexus preparation. Higher concentrations of the salt cause a progressive block of contractions. Sodium chloride shows no augmentation of contraction height, but concentrations above 10(-2)M only cause block of contractions. Inhibition of contractions by LiCl exactly parallels inhibition of responses of the tissue to exogenous acetylcholine (ACh); thus, the site of action is considered to be directly on the muscle. Sodium chloride causes insignificant inhibition of responses to exogenous ACh. Guinea-pigs injected chronically with high doses of LiCl (2 months, 5 mEq/kg show no stimulatory effect on LiCl in vitro, only inhibition. This finding suggests that tolerance to at least some of the actions of LiCl may occur upon chronic administration, particularly if the dose used is very high.

Acetylcholine↗

PubMed1980

Structure of the myenteric plexus in the sphincters of cat gastro-intestinal tract. V. Ultrastructure of the nerve cell bodies and dendrites.

A description is given of the nerve cell bodies and dendrites in the myenteric ganglia in the lower esophageal, pyloric and ileo-caecal sphincters of cats. The perikarya within one ganglion are differentiated depending on the position and predominance of one type of intracellular organelles or another. The question is raised whether these differences are a manifestation of the functional state, age characteristics or functional differentiation. The neurones in the myenteric plexus of the sphincters are characterized by the variety of dendrite branches, differing in shape and size.

Animals↗

PubMed1993

Analysis of the CCKB receptor antagonism of virginiamycin in guinea-pig ileum longitudinal myenteric plexus.

1. Virginiamycin, a macrolide reported to bind selectively to CCKB/gastrin receptors has been studied in a functional test, namely cholecystokinin-induced contraction of guinea-pig ileum myenteric plexus (LMMP). 2. Virginiamycin (1-10 microM) antagonized the selective CCKB agonist cholecystokinin tetrapeptide (CCK-4). The antagonism appeared not to be competitive as the highest concentration (10 microM) caused a reduction of its maximal effect. An apparent pA2 of 6.64 +/- 0.06 (s.e.) could be estimated if this depression was ignored. The selective CCKB antagonist, L-365,260 (0.01-0.3 microM) antagonized competitively the CCK-4 induced contraction and a pKB of 8.60 +/- 0.16 (s.e.) was estimated. 3. The combined dose-ratio analysis for virginiamycin, tested at 3 and 10 microM in association with 0.03 and 0.1 microM L-365,260, respectively, resulted in observed log dose-ratios of 1.39 and 1.53. That was consistent with both antagonists acting on the same receptor in LMMP. 4. These data, represent the first evidence of the antagonism of virginiamycin in a functional assay and they support the hypothesis of homogeneity between CCKB receptors in the CNS and in peripheral tissues.

Animals↗

PubMed1980

Structure of the myenteric plexus in the sphincters of cat gastro-intestinal tract. VI. Axonal profiles, axonal varicosities, synapses and other membrane differentiations.

Axonal varicosities of adrenergic, cholinergic and p-ergic types are observed in the myenteric plexus of cat lower esophageal, pyloric and ileo-caecal sphincters. In addition to them, there are varicosities, which cannot be attributed to the above types. The synaptic contacts in the myenteric ganglia manifest a great variety. The three main types of axonal varicosities appear as presynaptic part. Axodendritic synapses predominate. Very frequent findings are the symmetric membrane differentiations between the perikarya, dendrites and axonal profiles, as well as membrane junctions between the nerve and glial cells.

Animals↗

PubMed1992

Colocalization of nitric oxide synthase and NADPH-diaphorase in the myenteric plexus of the rat gut.

The pattern of distribution and colocalization of nitric oxide-synthase (NOS) and NADPH-diaphorase in the myenteric plexus of whole-mount preparations of the antrum, duodenum, ileum, caecum, proximal colon and distal colon of the rat were investigated using immunohistochemical and histochemical staining techniques. Almost all the myenteric neurons that were NOS-positive in all regions of the gut examined were also stained for NADPH-diaphorase. However, in the stomach, duodenum and ileum, only a few of the NOS-positive nerve fibres in the tertiary and secondary plexuses and circular muscle layer were also stained for NADPH-diaphorase, whereas in the caecum and distal colon almost all the NOS-positive nerve fibres were also stained for NADPH-diaphorase. The results in the present study are consistent with the view that nitric oxide (NO) has a mediating role in gastrointestinal neurotransmission.

Amino Acid Oxidoreductases↗

PubMed1997

Preliminary immunohistochemical new findings in the myenteric plexus of patients with intestinal neuronal dysplasia type B.

In order to investigate the causes of abnormal peristalsis of the colon in intestinal neuronal dysplasia (IND), we studied the structure of the myenteric plexus of IND colon using silver-impregnation (Suzuki's method) as well as the innervation of both IND colons and normal colons using immunofluorescence technique with monoclonal antibodies to synaptic vesicles, and antisera to vasoactive intestinal polypeptide (VIP), substance P (SP), methionine-enkephalin (Met-Enk), and gastrin-releasing peptide (GRP). The following results were obtained. 1) In the IND colon, the number of identifiable myenteric ganglia was decreased. In a few cases of IND, irreversible neuron degeneration can be involved in the pathogenesis of IND. 2) In the IND colon, the distribution and fluorescence intensity of synaptic vesicles coincided with those of peptidergic nerve fibers. In the normal colon, synaptic vesicles were much more numerous in the circular muscle layers than in the longitudinal muscle layers, and the fluorescence intensity of those in the circular muscle layers was stronger than that of those in the longitudinal muscle layers. On the other hand, in IND colon, there were fewer synaptic vesicles in the circular muscle layers, and their fluorescence intensity was weak, while there were many synaptic vesicles in the longitudinal muscle layers, and their fluorescence intensity was strong. 3) Morphological abnormalities may exist in synaptic vesicles in the circular muscle layers of the IND colon. 4) Regarding the peptidergic nerve fibers, in the IND colon, innervation of circular muscle layers by Met-Enk-, GRP- and SP-immunoreactive fibers was reduced, and longitudinal muscles were more strongly innervated by immunoreactive fibers than those in the normal colon. 5) Disturbed innervation of non-adrenergic non-cholinergic excitatory nerves may cause the disturbance of muscle contractions in the IND colon. In addition, an imbalance of peptidergic and synaptic vesicle's innervations in both muscle layers may be related to the abnormal peristalsis of IND colon. Also, morphological abnormalities of synaptic vesicles may be concerned with its abnormal peristalsis.

Adolescent↗

PubMed1995

A1-receptor-mediated effect of adenosine on the release of acetylcholine from the myenteric plexus: role and localization of ecto-ATPase and 5'-nucleotidase.

No attempt has been made so far to classify the subtypes of presynaptic inhibitory adenosine receptors located in the myenteric plexus and to localize ecto-ATPase and 5'-nucleotidase in the intestine. The release of [3H]acetylcholine and smooth muscle responses to acetylcholine were measured and the effect of selective adenosine receptor ligands was studied using field-stimulated isolated longitudinal muscle strips of guinea-pig ileum. Release of ATP and its hydrolysis rate were also measured using the luciferin-luciferase technique. A histochemical method combined with electron microscopy was used for localization of ecto-ATPase and 5'-nucleotidase, enzymes responsible for destruction of extracellular ATP, ADP and AMP. Subtype-selective A1-receptor agonists and antagonists inhibited and enhanced, respectively, the release of acetylcholine associated with neuronal activity. A significant amount of ATP was released in response to electrical stimulation and administration of carbamylcholine. The release of ATP was inhibited by atropine and 4-diphenylacetoxy-N-methylpiperidine methiodide, an M3-receptor antagonist. Hydrolysis of ATP was rapid and resulted in an accumulation of extracellular adenosine involved in presynaptic A1-receptor-mediated inhibition of acetylcholine release. While the inhibitory effect of adenosine and ATP was significantly potentiated by dipyridamol, an adenosine uptake blocker, that of 2-ms ATP was not. The effect of ATP was not competitively antagonized by 8-cyclopentyl-1,3-dipropylxanthine, a selective A1-receptor antagonist. In conclusion, axon terminals of cholinergic interneurons are equipped with inhibitory A1- and P2 gamma-receptors. Therefore, both adenosine and ATP control the release of acetylcholine through these receptors. ATP is mainly released from the smooth muscle in response to stimulation of M3-muscarinic receptors by endogenous acetylcholine (cascade transmission [Vizi E. S. et al. (1992) Neuroscience 50, 455-465]) and is rapidly hydrolysed by ecto-ATPase localized on the surface of the smooth muscle and axon terminals producing ADP and AMP, and by 5'-nucleotidase present only on the surface of smooth muscle cells producing adenosine.

5'-Nucleotidase↗