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At least 235 records · Page 13Linked to original sources
PubMed2000

Functional vagal input to gastric myenteric plexus as assessed by vagal stimulation-induced Fos expression.

Immunohistochemical detection of c-Fos expression was used to identify gastric myenteric plexus neurons that receive excitatory input from vagal efferent neurons activated by electrical stimulation of the cervical vagi in anesthetized rats. Vagal stimulation-induced Fos expression increased with higher pulse frequency, so that with 16 Hz (rectangular pulses of 1 mA/0.5 ms for 30 min) approximately 30% and with 48 Hz 90% of all neurons near the lesser curvature were Fos positive. In sham-stimulated rats there was no Fos expression. The percentage of Fos-activated neurons was only slightly smaller (85% with 48 Hz) near the greater curvature. Prior atropine administration (1 mg/kg ip) had little effect on vagal stimulation-induced Fos expression, and in unilaterally stimulated rats there was no Fos expression on the contralateral (noninnervated) side of the stomach, ruling out mediation by gastric motility or secretory responses. However, polysynaptic recruitment of third- and higher-order neurons cannot be ruled out completely. These results support the idea that, at least in the stomach, functional excitatory innervation of myenteric plexus neurons by the efferent vagus is profuse and widespread, refuting the notion of only a few vagal "command neurons."

Adjuvants, Anesthesia↗
PubMed2003

Actions of bradykinin on electrical and synaptic behavior of neurones in the myenteric plexus of guinea-pig small intestine.

1. Electrophysiologic methods were used to study actions of bradykinin (BK) in neurones of the myenteric plexus of guinea-pig small intestine in vitro. Exposure to BK depolarized the membrane potential and elevated excitability in AH- and S-type neurones. Neuronal input resistance associated with the depolarizing responses was either decreased or unchanged in S-type and increased in AH-type neurones. 2. The selective B(2) BK receptor antagonist HOE-140, but not the selective B(1) receptor antagonist des-arg(10)-HOE-140, suppressed the BK-evoked responses. RT-PCR confirmed the expression of B(2) receptor mRNA, but not B(1) receptor mRNA. 3. Binding of fluorescently- labeled HOE-140 (HOE741) was localized to ganglion cells in whole-mount preparations. BK B(2) receptors were coexpressed with immunoreactivity for calbindin or nitric oxide synthase. 4. Exposure to BK suppressed the amplitude of both fast and slow excitatory postsynaptic potentials. Depolarizing responses evoked by application of serotonin or substance P and nicotinic responses to acetylcholine were not reduced by BK. This suggested that BK action on neurotransmission was presynaptic suppression of neurotransmitter release. Presence of HOE-140 in the bathing solution suppressed or abolished the presynaptic inhibitory action of BK. 5. The cyclooxygenase inhibitor, piroxicam, suppressed both the direct excitatory action of BK and its presynaptic inhibitory action. Application of prostaglandin E(2), D(2), F(2alpha) or I(2) mimicked the BK-evoked responses. 6. The results suggest that BK acts at B(2) BK receptors on myenteric neurones to stimulate the formation of prostaglandins. Once formed and released, the prostaglandins act to elevate the excitability of ganglion cells in the myenteric plexus and to suppress the synaptic release of neurotransmitters.

Animals↗
PubMed1995

Stimulation-induced 3H-L-citrulline accumulation in isolated longitudinal muscle myenteric plexus preparations of rat small intestine: a measure to characterize nitrergic neurons.

Nitric oxide (NO) synthase activity in rat isolated longitudinal muscle myenteric plexus preparations of the small intestine was determine by measuring the accumulation of 3H-L-citrulline during 30 min incubation with 3H-L-arginine. In untreated preparations a significant amount of 3H-L-citrulline accumulated in the tissue, about 2000 dpm/30 mg per 30 min, accounting for about 1.7% of the tissue radioactivity. Intermittent electrical field stimulation (15 Hz, 10 s trains with 10 s intervals for total of 20 min) caused a threefold increase in 3H-L-citrulline accumulation. The NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) reduced the spontaneous accumulation of 3H-L-citrulline by 65% and prevented the electrically evoked increase. Removal of extracellular calcium or addition of tetrodotoxin blocked the electrically evoked increase in 3H-L-citrulline accumulation without affecting spontaneous accumulation. Application of the calcium ionophore A 23187 (10 mumol/l) or 45 mmol/l) or 45 mmol/l potassium caused a twofold increase in the accumulation of 3H-L-citrulline. The muscarine receptor agonist oxotremorine (1 mumol/l) had no effect on spontaneous accumulation of 3H-L-citrulline, but inhibited the electrically evoked increase by about 50%, and this effect was blocked by scopolamine. A substantial amount of 3H-L-citrulline (15000 dpm) accumulated also in the incubation media, and this was increased 1.7-fold by the presence of A 23187 and 2.7-fold by electrical stimulation. However, electrically evoked increase in 3H-L-citrulline was not prevented by tetrodotoxin, in contrast to observation on tissue levels. In conclusion, during incubation with 3H-L-arginine tissue levels of 3H-L-citrulline in rat isolated longitudinal muscle myenteric plexus preparations, but not accumulation in incubation media may be used as a biochemical marker of the activity of nitrergic intestinal neurons which appear to be inhibited via muscarine receptors.

Animals↗
PubMed1986

Pharmacological evidence for the existence of interactions between dopaminergic and opioid peptidergic systems in guinea-pig ileum myenteric plexus.

Apomorphine or bromocriptine treatment at doses that act on dopamine autoreceptors resulted in a significant elevation of the release of opioid peptides from the myenteric plexus of guinea-pig, since these drugs produced an increase of the inhibitory response which was reversed by naloxone. 6-Hydroxydopamine treatment also resulted in an increase in opioid peptide release. These findings would indicate that the 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 at this level.

Animals↗
PubMed1996

Effects of maternal proteic undernutrition on the neurons of the myenteric plexus of the duodenum of rats.

The purpose of this study was to verify the effects of proteic undernutrition on the neurons of the myenteric plexus from the duodenum of Wistar rats. Twenty-four animals at the age of 60 days were divided in four groups, which were named according to the period their mothers received hypoproteic ration (8%). Some segments of duodenum were subjected to histological treatment and stained with hematoxilin-eosin and some were used for whole mount preparations stained with Giemsa. We observed small, medium-sized and large neurons grouped in ganglia of various shapes. It was concluded that the maternal proteic undernutrition does not affect the organization of the myenteric plexus and that animals submitted to undernutrition during gestation and lactation, when normally fed, show neurons with strongly basophilic cytoplasm and larger cellular bodies than those from control animals.

Animals↗
PubMed1985

Neurons dissociated from rat myenteric plexus retain differentiated properties when grown in cell culture. I. Morphological properties and immunocytochemical localization of transmitter candidates.

We have developed procedures for dissociating neurons from the myenteric plexus of the small intestine of newborn rats and for growing those neurons in cell cultures for up to 3 months. Neurons in these cultures retain many of the differentiated properties of myenteric neurons in vivo. This is the first of a series of 3 papers describing those properties. In this paper, we describe the morphology of cultured neurons that we have observed with light and electron microscopy; we also describe the patterns of straining observed when immunocytochemical techniques were used to localize neurotransmitter candidates in the cultured neurons. Intracellular injections of a fluorescent dye, Lucifer yellow, revealed that many of the cultured neurons had morphologies similar to those of myenteric neurons in vivo. When thin sections of cultures were viewed in an electron microscope, many neurons were observed to have numerous small (40-60 nm), clear synaptic vesicles and/or large (80-150 nm), opaque-cored (p-type) vesicles. Synaptic profiles were most often observed on neuronal somata. Neurons containing immunoreactive serotonin, substance P, somatostatin, enkephalin, bombesin and gastrin/cholecystokinin were observed in about the same proportions as they occur in the intact myenteric plexus. Neurons containing immunoreactive vasoactive intestinal polypeptide were found in higher numbers than reported in vivo. Neurons containing immunoreactive neurotensin, secretin and glutamate decarboxylase were not observed. An antiserum directed against choline acetyltransferase stained 40-50% of the neurons. We conclude that myenteric neurons continue to express much of their normal differentiated properties even when they are removed from the gut, dissociated into a suspension of single cells and grown in culture. Such cultures will be useful for correlating the morphological, biophysical, pharmacological and synaptic properties of individual myenteric neurons and for testing the ability of altered environmental conditions to change those properties.

Animals↗
PubMed1985

Pre-incubation of guinea-pig myenteric plexus with beta-funaltrexamine: discrepancy between binding assays and bioassays.

The acute effects of beta-funaltrexamine and the effects of pre-incubation with this compound were examined in five in vitro assay tissues and in selective binding assays in homogenates of guinea-pig brain and myenteric plexus. In competitive displacement assays with selective ligands, beta-funaltrexamine had highest affinity for the mu-binding site in the myenteric plexus and brain of guinea-pig. Its affinity for the kappa-site was about 15% of that for the mu-site. Pre-incubation of the assay tissues with beta-funaltrexamine caused an increase in the IC50 values of mu- and delta-receptor agonists but not of kappa-agonists. Although in bioassays on the myenteric plexus-longitudinal muscle preparation of the guinea-pig, the IC50 value of the mu-receptor ligand [D-Ala2, MePhe4, Gly-ol5] enkephalin was increased up to 124 fold, its binding at the mu-site in homogenates of the preparation was not affected by this treatment. These findings indicate that the effects of pre-incubation with beta-funaltrexamine on agonist potency of the mu-receptor ligand are due to an interference with the coupling mechanism between the mu-binding site and the effector system.

Animals↗
PubMed1979

Comparison of binding of [3H]-methionine-enkephalin, [3H]-naltrexone and [3H]-dihydromorphine in the mouse vas deferens and the myenteric plexus and brain of the ginea pig.

[3H]-Methionine-enkephalin, [3H]-naltrexone and [3H]-dihydromorphine are specifically bound in homogenates of not only the brain and myenteric plexus of the guinea pig but also the vas deferens of the mouse. Brain has a ratio of methionine-enkephalin to dihydromorphine binding in favour of methionine-enkephalin binding and the myenteric plexus a ratio in favour of dihydromorphine binding, with the mouse vas deferens being intermediate.

Animals↗
PubMed1984

Myenteric plexus in streptozotocin-treated rats. Neurochemical and histochemical evidence for diabetic neuropathy in the gut.

Adrenergic, cholinergic, and serotoninergic nerves were studied in the myenteric plexus of ileum and colon from streptozotocin-treated rats, an animal model of juvenile-onset diabetes. In view of clinical reports implicating diabetic autonomic neuropathy as the cause of gastrointestinal dysfunction in diabetes mellitus, neurochemical and histochemical techniques were used to study changes in the innervation of the gut. In the myenteric plexus of the ileum from diabetic animals, adrenergic nerves displayed signs of degeneration and the brightness of fluorescence in serotoninlike immunoreactive nerves was lower. Cholinergic nerves, however, did not display any signs of reduction in the ileum, and both choline acetyltransferase and acetylcholinesterase activities per centimeter were increased. In contrast, in the proximal colon 8 wk after induction of diabetes, neurochemical assays revealed significant increases in noradrenaline and serotonin levels as well as choline acetyltransferase activity, although no obvious changes in the pattern of innervation could be detected histochemically. The results indicate that changes do occur in the innervation of the gut of the streptozotocin-diabetic model shortly after the induction of diabetes, although they differ significantly in the ileum and colon; these may be of relevance to the types of gastrointestinal dysfunction displayed in human diabetes.

Animals↗
PubMed1990

Ultrastructure and synaptology of neurons immunoreactive for gamma-aminobutyric acid in the myenteric plexus of the guinea pig small intestine.

Immunoreactivity for gamma-aminobutyric acid is located in one morphologically-defined class of nerve cell body in the myenteric plexus of the guinea pig small intestine. These are a subgroup of the Dogiel type I nerve cells, characterized by their lamellar dendrites, about 1 micron thick and flattened in the plane of the myenteric plexus, and one (or rarely two) long axonal process that extends to either the longitudinal or the circular muscle. At an ultrastructural level the dendrites were characterized by their open cytoplasm in which were scattered granular vesicles, pale mitochondria, Golgi apparatus and endoplasmic reticulum. A large proportion of the dendritic surface was in direct contact with the extra-ganglionic space. In the cell body region, which was away from the ganglion surface, the nucleus was surrounded by a thin rim of cytoplasm. The cytoplasmic features are quite distinct from those of Dogiel type II neurons but they were shared by many other non-immunoreactive neurons. Synaptic inputs, which were all non-immunoreactive, were found on the dendrites, cell bodies, axon hillocks and axons of the gamma-aminobutyric acid-immunoreactive neurons. The predominant vesicle type in the presynaptic elements was the small clear vesicle, 40-60 nm in diameter. Based on two gamma-aminobutyric acid-immunoreactive cells that were examined in serial section, about 40-50% of synapses are dendritic, 20-25% are somatic, and 30-35% are on the axon hillock or first 50-70 microns of the axon. No synapses formed by immunoreactive varicosities were found on non-immunoreactive neurons or in the neuropil of the myenteric ganglia. Moreover, the lamellar dendrites or soma of gamma-aminobutyric acid neurons were never presynaptic elements forming relationships with other elements in the ganglia. It is concluded that the gamma-aminobutyric acid reactive Dogiel type I neurons are motor neurons providing inputs to the circular and longitudinal muscle layers.

Animals↗
PubMed1985

Cytodifferentiation of the interstitial cells of Cajal related to the myenteric plexus of mouse intestinal muscle coat. An E.M. study from foetal to adult life.

The cytodifferentiation of the interstitial cells of Cajal (Type I) related to the myenteric plexus of the mouse intestinal muscle coat was studied in foetuses at term, neonates not yet fed, suckling animals, weaning animals and adult animals. In foetuses at term, interstitial cells of Cajal and their precursor cells are not identifiable. In neonates not yet fed, presumed precursor cells of the interstitial cells of Cajal, i.e. ICC-blasts, can be identified as cells surrounding the developing myenteric plexus and interposed between the circular and longitudinal muscle layers. These ICC-blasts are poorly differentiated but, like the adult interstitial cells, are always related to nerve endings and possess large and numerous mitochondria. In suckling animals these cells gradually develop, and are fully differentiated only after the end of the weaning period.

Animals↗
PubMed1995

Effects of H-89, an inhibitor of protein kinase A, on the acetylcholine release from myenteric plexus of guinea pig ileum.

In order to clarify the involvement of cyclic AMP-dependent protein kinase (protein kinase A) in acetylcholine (ACh) release from myenteric plexus of guinea pig ileum, the effect of H-89, a specific inhibitor of protein kinase A, on the ACh release was investigated. H-89 (0.1-10 microM) inhibited the spontaneous and nicotine-induced release of ACh in a concentration dependent manner. It at 1 microM decreased both kinds of release of ACh to almost half of the control, but it did not affect the ACh release evoked by electrical field stimulation and by 5-hydroxytryptamine. H-89 had no significant effect on the indomethacin (IND), an inhibitor of PG synthesis, -insensitive component of the spontaneous and nicotine-induced release of, ACh. OP-41483, an analog of PGI2 and forskolin, an activator nicotine-induced release of, ACh. OP-41483, an analog of PGI2 and forskolin, an activator of adenylate cyclase, reversed the inhibitory effect of IND on the ACh release. H-89 at 1 microM completely inhibited the reverse effects of OP-41483 and forskolin. These results suggest that activation of protein kinase A is essential for modulation of the nicotine-induced and spontaneous ACh release from myenteric plexus of guinea pig ileum and the activity of protein kinase A is regulated by endogenous PGs via intracellular cyclic AMP level.

Acetylcholine↗
PubMed1995

Analysis of connections between nitric oxide synthase neurons in the myenteric plexus of the guinea-pig small intestine.

In the myenteric plexus of the guinea-pig ileum, a sub-population of descending interneurons contains nitric oxide synthase. Final neurons in descending motility pathways, inhibitory circular muscle motor neurons, also contain nitric oxide synthase. In this study we used ultrastructural immunocytochemistry to determine whether nitric oxide synthase descending interneurons provide inputs to all nitric oxide synthase neurons. The presence of nitric oxide synthase inputs to 35 nitric oxide synthase nerve cells from three animals was examined. Nine nerve cells from one ganglion were studied in serial section. Every nerve cell received inputs (close contacts and synapses) from nitric oxide synthase terminals. The number of inputs to the nine serially sectioned neurons ranged from 13 to 45. The inputs were found in about equal numbers on the cell bodies and the dendrites. There was no significant correlation between the size of nitric oxide synthase neurons and the number of nitric oxide synthase inputs they received. There was also no correlation between the number of nitric oxide synthase inputs and the number of 5-hydroxytryptamine inputs (determined in a previous study) received by nitric oxide synthase neurons. Random sections through an additional 26 nitric oxide synthase neurons (seven in the same ganglion and 19 from another two myenteric ganglia from different animals) were examined and nitric oxide synthase synapses and close contacts were observed on each neuron. Nitric oxide synthase interneurons and motor neurons are morphologically indistinguishable.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1980

Changes in the neuronal activity of the ganglia of the myenteric plexus upon transmural electrical stimulation.

The neuronal activity of the myenteric plexus is recorded extracellularly in preparations isolated from cat duodenum, using tungsten microelectrodes with tip diameter 5-10 micrometers and resistance 0.5-2 mOhms. Transmural electrical stimulation after Burn and Rand (1960) with a pair of platinum electrodes is applied at a distance of 1 cm proximally from the place of recording. The responses of the single-spike neurones and of the erratic burst-type neurones to transmural electrical stimulation (series of impulses with frequency 1-20 Hz, duration of impulses 0.1-0.5 ms and suprathreshold current intensity) depend on the background neuronal activity. Thus, in the case of weak activity, stimulation with a frequency of 1-8 Hz results in activation of both types of neurones. A particularly high neuronal activity, stimulation with the same frequency results in inhibition. Transmural electrical stimulation does not change the character of the activity of steady burst-type neurones.

Action Potentials↗
PubMed1993

Role of prostacyclin in acetylcholine release from myenteric plexus of guinea-pig ileum.

The roles of metabolites of arachidonic acid in spontaneous and agonist-induced acetylcholine release from a longitudinal muscle preparation with myenteric plexus of guinea-pig ileum were studied. Indomethacin significantly decreased both spontaneous acetylcholine release and its release induced by nicotine and substance P. We had found that prostaglandin E2 (PGE2) partly reversed this inhibition. We now found that a stable prostacyclin analog, OP-41483 at 100 nM, completely reversed the inhibition of acetylcholine release by indomethacin. On the other hand, PGD2, PGF2 alpha and ONO-11113, a thromboxane A2 analog, did not have any significant effect on the inhibition by indomethacin. OP-41483 had no effect on acetylcholine release induced by nicotine or substance P in the absence of indomethacin. To confirm the modulatory role of endogenous prostaglandins on acetylcholine release, we also studied the release of 6-keto-PGF1 alpha, a metabolite of prostacyclin, and PGE2 from longitudinal muscle preparations. The preparations released appreciable amounts of 6-keto-PGF1 alpha continuously during the experiments. Indomethacin inhibited release, while nicotine did not affect it so significantly. Our results suggest that endogenous prostacyclin modulates acetylcholine release from cholinergic nerve terminals in the myenteric plexus of guinea-pig ileum.

Acetylcholine↗
PubMed1994

Morphology of horseradish peroxidase (HRP)-injected glial cells in the myenteric plexus of the guinea-pig.

Glial cells of the myenteric plexus from guinea pig small intestine were intracellularly filled with horseradish peroxidase (HRP), and histochemically stained. Camera lucida-like drawings of twenty cells were morphologically and morphometrically analyzed. The cells have very small ellipsoid somata (8.5 +/- 0.7 microns equivalent diameter, i.e., about 330 micron3 volume), and send up to 20 thin and short processes (less than 26 to about 110 microns in length). The morphology of the cells appears to depend on their location within the plexus. Glial cells located within the ganglia are similar to CNS protoplasmic astrocytes; they are star-shaped, and their very short processes are irregularly branched. In contrast, glial cells within the interganglionic fiber tracts resemble CNS fibrous astrocytes. They extend longer processes that are parallel to the fiber tracts, and show less tendency to branch. We propose that the morphology of enteric glia is determined by the structure of the microenvironment. Both cell types form several flat endfeet at a basal lamina either surrounding blood vessels or at the ganglionic border. Furthermore, the occurrence of "holes" in the glial cell processes suggests that particular neuronal cell processes may be enwrapped in a specific manner. Fractal analysis of camera lucida-like drawings of the cells showed that the cells have a highly complex surface structure, comparable to that of protoplasmic astrocytes in the brain. These tiny cells may possess a membrane surface area of approximately 2000 micron2, almost 90% of which are contributed by the cell processes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Acute and chronic effects of opiates on single neurons of the myenteric plexus.

Extracellular recordings were made from single neurons in the myenteric plexus of the guinea-pig ileum in vitro. Tissue was removed from morphine-naive guinea pigs and maintained in vitro for up to 24 hr; the firing rate of the neurons was reduced by opiate agonists and unaffected by opiate antagonists. Tissues were also removed from animals which had been pretreated with morphine during 3 days and placed into an in vitro solution which contained morphine. An increase in the concentration of morphine did not inhibit neuronal firing and naloxone caused a pronounced excitation of such cells. Cross-tolerance among different opiate agonists was apparent. In a third experiment, tissues were removed from morphine-naive guinea pigs and incubated in vitro for 24 hr in a solution which contained an opiate agonist. An increase in the concentration of agonist did not inhibit cell firing and opiate antagonists caused marked excitations of neurons incubated with morphine. Incubation with opiate agonists induced a much reduced sensitivity to the inhibitory effect of morphine on cell firing (tolerance) and also sensitized the cells to a marked excitatory effect of opiate antagonists (dependence) which was similar to the changes induced by in vivo opiate administration. The changes induced by morphine during 24 hr in vitro were not affected by the concomitant presence of sufficient lidocaine to prevent neuronal activity.

Action Potentials↗