PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “MYENTERIC PLEXUS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMed1985

Presynaptic modulation by noradrenaline and an opioid of the substance P-induced release of [3H]acetylcholine from the myenteric plexus.

Substance P (7.5-750 nM) applied in superfusion dose-dependently released 3H from isolated strips of myenteric plexus-longitudinal muscle of the guinea-pig ileum loaded with [3H]choline. Separation of the [3H]acetylcholine and [3H]choline components of the released radioactivity revealed that in response to substance P (SP) administration only the release of [3H]acetylcholine increased above resting level. A slowly developing tachyphylaxis to the effect of SP was observed. Evidence has been obtained that the slow tachyphylaxis developed to the acetylcholine-releasing effect of SP was not due to the exhaustion of releasable acetylcholine pool. Release of acetylcholine by 150 nM SP was completely prevented by tetrodotoxin or in a Ca2+-free medium and greatly reduced in the presence of noradrenaline or the opioid receptor agonist (D-Met2,Pro5)-enkephalinamide. The effect of noradrenaline and the opioid peptide was apparently prevented by yohimbine and naloxone, respectively.

Acetylcholine↗
PubMedDate not supplied

Bradykinin releases acetylcholine from myenteric plexus by a prostaglandin-mediated mechanism.

Release of [3H]acetylcholine (ACh) under the influence of bradykinin was measured from myenteric plexus-longitudinal muscle strips taken from guinea pig small intestine. Bradykinin stimulated the efflux of [3H]ACh in a dose-dependent manner. This stimulation by bradykinin was resistant to the effect of [Des-Arg9-Leu8]-bradykinin but not to indomethacin, indicating that the ACh-releasing action of bradykinin was mediated indirectly by a prostaglandin mechanism. Direct evidence for a stimulation of ACh release by prostaglandin E1 was obtained. Prostaglandin was able to stimulate ACh release in a dose-related fashion. The inhibition of bradykinin-induced ACh release by indomethacin was partly reversed by exogenous prostaglandin E1. These results suggest a neuromodulatory role for bradykinin in the enteric nervous system.

Acetylcholine↗
PubMed1983

Ontogenesis of the myenteric plexus in the cat gastrointestinal sphincters. III. Synaptogenesis.

Synaptogenesis in the cat myenteric ganglia of the lower esophageal, pyloric and ileocecal sphincters in the fetal life and at different postnatal stages of development was examined. The synaptic formation began in the early fetal period. The first immature synapses were of axosomatic and axodendritic types. The new formation and maturation of the synaptic contacts was an active process in the fetal period and in the first postnatal weeks, but it continued to the adult level. It was expressed quantitatively in the increase of the surface area of the synaptic contact zones, the number of the synapses, the length of the synaptic contact zones and the number of the synaptic vesicles. Fine structural features of the synaptic maturation were the increased pleomorphism of the synaptic vesicles, widing and lengthening of the thickening of the opposed membranes, the appearance of the coated evaginations and vesicles. Synaptic morphology became more complex because of the including of different in size and structure pre- and postsynaptic components. The frequency of the synapses on dendritic spines and synapses "en passant" increased. The synaptogenesis in the three sphincters studied exhibited a different dynamics. The parallel advance in the neuronal and synaptic differentiation and the relationship between the desmosomal junctions and synapses were discussed.

Animals↗
PubMed1985

Effects of adenosine on 45Ca uptake and [3H]acetylcholine release in synaptosomal preparation from guinea-pig ileum myenteric plexus.

The effects of adenosine on acetylcholine (ACh) release and calcium uptake were examined in a synaptosomal fraction prepared from guinea-pig ileum myenteric plexus-longitudinal muscle. A high concentration of potassium (40 mM) and electrical pulses (ES:10Hz) caused a marked increase in the output of [3H]ACh from [3H]choline-preloaded crude synaptosomes. This [3H]ACh output was calcium- and temperature-dependent. Adenosine reduced the high potassium-induced release significantly, and the electrically stimulated release completely. When the preparation was depolarized by high potassium or electrical pulses, the 45Ca uptake by synaptosomes was significantly enhanced. The uptake of 45Ca induced by high potassium was significantly reduced and that induced by electrical stimulation was completely abolished by adenosine. From these results, it may be suggested that adenosine inhibits neurotransmitter release by suppressing the presynaptic influx of calcium ion during depolarization of the cholinergic nerve terminals in guinea-pig ileum.

Acetylcholine↗
PubMed1981

A synaptosomal preparation from the guinea pig ileum myenteric plexus.

Our interest in investigating the presynaptic modulation of acetylcholine release led to the development of a synaptosomal preparation from the guinea pig ileum myenteric plexus-longitudinal muscle. A crude synaptosomal fraction (P2) was obtained by homogenization and differential centrifugation. The preparation exhibited a specific uptake system for choline and for noradrenaline (NA), but not for 5-hydroxytryptamine (5-HT). Synaptosomes were isolated from this P2 fraction by an isoosmotic density gradient prepared from sucrose and metrizamide. The resultant synaptosomal fraction was enriched about sevenfold in both choline uptake and in choline acetyltransferase (ChAT). Choline was transported by a high-affinity system was a Km of 6.5 X 10(-7) M and a Vmax of 41 pmol/mg protein/min. Electron microscopy confirmed the synaptosomal nature of the gradient fraction. Some synaptosomal profiles contained only small, translucent vesicles whereas others also contained large (approx. 100 nm diameter) electron-opaque vesicles. The crude synaptosomal fraction synthesized acetylcholine (ACh) from exogenous choline and it released the synthesized ACh in a calcium-dependent manner.

Acetylcholine↗
PubMed1981

Tetraethylammonium facilitates the stimulation-evoked loss of the enkephalins from the myenteric plexus of guinea-pig ileum.

The effects of electrical field stimulation on the contents of [Met]enkephalin and [Leu]enkephalin were determined in myenteric plexus-longitudinal muscle preparations of the guinea-pig small intestine. Cycloheximide (0.1 mM) was present in all experiments to prevent de nouveau biosynthesis. The two enkephalins were separated by high performance liquid chromatography and assayed on the mouse vas deferens. Stimulation with submaximal pulses (50 mA, 0.5 ms) at a frequency of 10 Hz caused maximal losses of about 35% of [Met]enkephalin and [Leu]enkephalin after 3 h (108000 pulses). The plot of log (enkephalin content) against number of pulses was steeper during the first 30 min than during the later periods. Tetraethylammonium bromide (TEA, 10 mM) increased the [Met]enkephalin and [Leu]enkephalin contents of the non-stimulated preparations by about 50%. When the preparations were stimulated in the presence of TEA at 50 mA and 1 Hz, the plots of loss of enkephalins against number of pulses were linear until the maximum of about 50% was reached. Compared with stimulation in the absence of TEA, the rate constant was 8 times greater for [Leu]enkephalin and 20 times greater for [Met]enkephalin. The absolute losses per pulse were about 13 times greater for [Leu]enkephalin and 27 times greater for [Met]enkephalin than in the absence of TEA. In the presence of bacitracin and a mixture of dipeptides, the enzymatic degradation of the enkephalins was sufficiently suppressed to cause an overflow of 30-60% of the enkephalins lost from their stores into the perifusing Krebs solution. Until it is possible to determine the preformed precursors, which are present in large quantities, the kinetics relationship between these precursors and the enkephalins cannot be investigated. A similar dilemma exists for the relationship between "released' enkephalins and the losses from their stores.

Animals↗
PubMedDate not supplied

Microdissection study of the myenteric plexus in acardia, ataxia-telangiectasia, cystic fibrosis, extrahepatic biliary atresia, pediatric AIDS and Werdnig-Hoffmann disease.

Microdissection-point count morphometric study of the myenteric (Auerbach) plexus or esophagus, small intestine, and colon was done for infants and children with acardia (2), ataxia-telangiectasia (5), cystic fibrosis of the pancreas (CFP) (25), extrahepatic biliary atresia (EBA) (17), pediatric AIDS (10), and Werdnig-Hoffmann disease (WHD) (8). Values for fractional area of neural tissue in the plane of the plexus were compared to those of control patients in same age range as those in each disease category by t-test. Statistically abnormal values included low values for small intestine and colon in Werdnig-Hoffmann disease, high values for small intestine and colon in biliary atresia, and high value for colon but a low value for small intestine in cystic fibrosis. Values for all three loci were within the normal range for ataxia telangiectasia and pediatric AIDS. The mechanisms of the low value for small and large intestines in WHD, which causes chronic constipation as a result of skeletal muscle weakness, and of the high values for colon in CFP and EBA, both causing malabsorption with bulky stools, are unclear. The value for small intestine in acardia was normal for term but lower than expected for fetal bowel of the same size, possibly because of reduced neural crest inflow to the fetal bowel.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Glucose-induced ion secretion in rat jejunum: a mucosal reflex that requires integration by the myenteric plexus.

We tested the hypothesis that the mucosa of rat jejunum is stimulated by intraluminal D-glucose, resulting in nerve-mediated ion secretion. We examined the D-glucose-induced secretory response in two ways. First, we measured the unidirectional fluxes of sodium and chloride ions, in vivo, during perfusion of segments of jejunum with solution that contained either D-glucose or mannitol. Second, we measured the net rate of absorption of D-glucose from sodium-free solution; this parameter is related to the rate of sodium ion secretion. We used the above two approaches in conjunction with techniques for destroying specific subsets of the intestinal nerves. Thus, we evaluated the subset of intestinal nerves that integrates the secretory response of the mucosa to D-glucose. Jejunal segments perfused with D-glucose solution exhibited significantly greater rates of sodium and chloride ion secretion than did segments perfused with mannitol. Intestinal segments in which the myenteric nerve plexus had been destroyed exhibited a significantly lower rate of sodium ion secretion in the presence of D-glucose than was seen in fully innervated segments. A role for the myenteric nerves in D-glucose-induced ion secretion was also indicated by experiments that involved absorption of D-glucose from sodium-free solution. It was concluded that exposure of the mucosa of rat jejunum to glucose increases the rate of secretion of both sodium and chloride ions. The myenteric nerve plexus is apparently involved in the integration of this mucosal reflex.

Animals↗
PubMed1976

Dependence liability of enkephalin in the myenteric plexus of the guinea pig.

The endogenous ligands of opiate receptors, methionine-eukephalin and leucine-enkephalin, were tested for their ability to maintain or to reinduce dependence in myenteric plexus-longitudinal muscle strips taken from tolerant/dependent guinea pigs. Both peptides fully substituted for the function morphine exerts in this preparation. It is concluded that the enkephalins posses a high degree of dependence liability.

Animals↗
PubMed1989

The effect of crotoxin on the longitudinal muscle-myenteric plexus preparation of the guinea pig ileum.

The effects of crotoxin, the neurotoxin of the venom of the South American rattlesnake (Crotalus durissus terrificus), was studied by using the myenteric plexus-longitudinal muscle preparation of the guinea pig ileum. Crotoxin (0.02-4.0 microM) caused depression of the twitch response of the electrically stimulated preparation. This transitory depression depended on the concentration of crotoxin; since crotoxin diminished the output of acetylcholine, this depression may be due to the inhibition of the release of acetylcholine from the plexus. Crotoxin also induced an early contraction, followed by relaxation; as the contraction was inhibited by aspirin and indomethacin, it may have resulted from the release of prostaglandin. In addition, a late persistent contracture was observed after the early contraction. The contracture was resistant to blockage by muscarinic, histamine and serotonin antagonists, to hexamethonium, a non-depolarizing ganglionic blocking substance and to tetrodotoxin, a sodium channel blocker. The contracture was blocked by an elevated concentration of calcium (10 mM) and by verapamil, a calcium channel blocker.

Acetylcholine↗
PubMed1988

Selective depletion of the acetylcholine and vasoactive intestinal polypeptide of the guinea-pig myenteric plexus by differential mobilization of distinct transmitter pools.

The effect of electrical field stimulation on the release of acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) from superfused strips of myenteric plexus-longitudinal muscle (MPLM) of guinea-pig ileum and on the transmitter content of the tissue was investigated at different frequencies and in the presence and absence of choline hemicholinium-3 and colchicine. Low frequency electrical field stimulation released ACh by more than 4 times the basal release; the simultaneously detected VIP secretion was increased only slightly above the resting level. During high frequency stimulation (50 Hz) the release of VIP was greatly increased (to 5 times the resting release) whereas the release of ACh increased to only 150% of the basal output. When choline was present, the ACh content of the tissue itself was not altered by electrical stimulation indicating a rate of synthesis sufficient to maintain release. It was reduced in a frequency-dependent manner in the absence of exogenous choline or in the presence of 10 microM hemicholinium-3 (an inhibitor of choline uptake) by up to 54% of the original content. A similar but even larger reduction took place in the amount of ACh released. Neither the secretion of VIP nor the tissue VIP content was altered by these treatments. Long-lasting (greater than 60 min) high-frequency (50 Hz) stimulation resulted in the depletion of the VIP pool (by 25%) while the ACh content remained unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1984

Release of endogenous 5-hydroxytryptamine from the myenteric plexus of the guinea-pig isolated small intestine.

The presence of 5-hydroxytryptamine (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in, and the release of these substances from, the myenteric plexus-longitudinal muscle (MPLM) layer of the guinea-pig isolated small intestine were investigated. 5-HT and 5-HIAA were measured by high performance liquid chromatography and electrochemical detection. Freshly prepared MPLM contained measurable amounts of 5-HT and 5-HIAA. For the release experiments, the MPLM was incubated in a medium containing the 5-HT uptake inhibitor fluoxetine and the monoamine oxidase inhibitor nialamide; this led to a decrease in the 5-HIAA content of the MPLM whereas the 5-HT content remained unchanged. There was a spontaneous release of 5-HT and 5-HIAA from the MPLM. The release of 5-HT was so small that it was just detectable; it seemed equivalent to about 0.8% of the tissue stores released per min. Depolarization of the tissue by increasing the [K+] or by exposing it to veratridine enhanced the release of 5-HT in a Ca2+-dependent manner whereas the release of 5-HIAA was not increased. Tetrodotoxin inhibited the veratridine-evoked release of 5-HT but did not affect the K+-evoked release of 5-HT. The presence of 5-HT in myenteric neurones and the characteristics of the release of 5-HT from these neurones strongly support the hypothesis that 5-HT is an enteric neurotransmitter.

Animals↗
PubMed1982

beta-Endorphin proteolysis by guinea-pig ileum myenteric plexus membranes: increased gamma-endorphin turnover after chronic exposure to morphine.

The influence of chronic morphine exposure in vitro on the biotransformation of beta-endorphin (beta E) was investigated using the myenteric plexus-longitudinal muscle of guinea-pig ileum. A membrane preparation was incubated with beta E and the degradation of beta E as well as the accumulation of several beta E fragments in the incubation medium were followed with time. The levels of peptides were determined by specific radioimmunoassays after separation by high-pressure liquid chromatography. It was found that exposure to morphine did not affect the disappearance of beta E, but altered the time course of accumulation of beta E fragments. In fact, the accumulation of gamma-endorphin, alpha-endorphin and des-tyrosine1-alpha-endorphin was enhanced, while that of des-tyrosine1-gamma-endorphin was not change. Additionally, the disappearance of gamma-endorphin appeared to be stimulated by morphine exposure. These data provide evidence that the fragmentation of beta E is changed by chronic morphine exposure in such a way that the turnover of gamma-endorphin is increased.

Animals↗