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PubMed1993

Intracellular calcium changes associated with cholinergic nicotinic receptor activation in cultured myenteric plexus neurones.

Intracellular free calcium concentration ([Ca2+]i) was measured in cultured explants of myenteric plexus neurones by using the fluorescent calcium indicator Indol in combination with patch-clamp techniques. The basal [Ca2+]i was 94 nM and spontaneous oscillations in the internal free calcium concentration were recorded. These oscillations were associated with bursts of action potentials triggered by spontaneous nicotinic excitatory synaptic potentials. Under voltage clamp conditions, application of the selective nicotinic agonist m-hydroxyphenylpropyl-trimethylammonium iodide (10 microM) induced an inward current and increased the intracellular free calcium concentration. We conclude that cholinergic synaptic excitatory activity provide a regular calcium entry in myenteric neurone and suggest that the nicotinic channel might be significantly permeable to calcium.

Animals↗

PubMed1993

Varicella-zoster virus DNA in the oesophageal myenteric plexus in achalasia.

In a search for past or present infection with herpes viruses, serum antibody titres to herpes simplex type 1 virus, cytomegalovirus, and varicella-zoster virus were measured by complement fixation test in 58 patients with achalasia. Serum was also taken from 40 age and sex matched patients without oesophageal symptoms who formed a control group. All titres were low, and those for herpes simplex type 1 virus and cytomegalovirus did not differ in the achalasia patients and the controls. However, the incidence of varicella-zoster virus antibodies was significantly greater in the achalasia than in the control group (p < 0.05). Using oesophageal tissue containing myenteric plexus removed at the time of cardiomyotomy in nine patients with achalasia, in situ DNA hybridisation showed evidence of varicella-zoster virus in three, but all were negative for the other two viruses. No positive results were obtained for herpes simplex type 1 virus, cytomegalovirus, or varicella-zoster virus in oesophageal tissue from 20 patients undergoing oesophageal resection for diseases other than achalasia. The incidence of positivity for varicella-zoster virus was significantly increased in the achalasia group compared with the controls (p < 0.02). The findings indicate that varicella-zoster virus DNA may persist in the oesophageal myenteric plexus in some patients with achalasia and raise the possibility that this virus is of aetiological importance in achalasia.

Adolescent↗

PubMed1981

Mediators of slow synaptic potentials in the myenteric plexus of the guinea-pig ileum.

1. Intracellular recordings were made from neurones in the myenteric plexus of the ileum isolated from adult guinea-pigs.2. Three synaptic potentials were evoked in different myenteric neurones by focal stimulation of the ganglion surface at a distance of up to 100 mum from the cell body from which the recording was made. These were the fast cholinergic excitatory post-synaptic potential (e.p.s.p.), the slow e.p.s.p. and the slow inhibitory post-synaptic potential (i.p.s.p.).3. 5-hydroxytryptamine and substance P were applied to the neurones by superfusion (10 nm-1 mum) or by electrophoresis within 5 mum of the neurone cell body. 5-HT depolarized, hyperpolarized or had no effect on approximately equal numbers of neurones, whereas substance P depolarized 90% of neurones.4. Many neurones with a depolarizing slow e.p.s.p. were hyperpolarized by superfusion or electrophoretic application of 5-HT.5. Superfusion with 5-HT reversibly depressed the fast e.p.s.p., slow e.p.s.p. and slow i.p.s.p. Superfusion with substance P depressed the slow e.p.s.p.6. Methysergide (10-30 mum) reduced the amplitude of the fast e.p.s.p., the slow e.p.s.p. and the slow i.p.s.p.7. Chymotrypsin (200 mug/ml.) reversibly reduced the amplitude of the slow e.p.s.p., but had no effect on membrane potential, the action potential or the fast e.p.s.p. Chymotrypsin reduced or abolished the depolarization caused by electrophoretic application of substance P, but had no effect on the depolarization or hyperpolarization caused by 5HT.8. The results provide evidence that 5-HT is not the transmitter which mediates the slow e.p.s.p. in myenteric neurones. The slow e.p.s.p. may be caused by substance P or another similar peptide.

Animals↗

PubMed1982

Role of calcium in muscarinic autoinhibition of 3H-acetylcholine secretion in guinea-pig ileum myenteric plexus.

The stores of acetylcholine (ACh) of the cholinergic neurons of guinea-pig myenteric plexus were labelled by preincubation with 3H-(methyl)-choline, to examine the dependence of the secretory mechanisms in these nerves, and of their muscarinic 'autoinhibition', on the extracellular calcium concentration. The curves describing the secretion of labelled transmitter evoked by electrical field stimulation at 1 Hz, as a function of external calcium, were essentially hyperbolic, except at very low calcium levels. Double reciprocal plots of the secretory responses vs. the external calcium concentration, within the 2-8 mM range, yielded straight lines, permitting estimation of apparent VmaxCa (height of asymptote parallel to abscissa = the maximal secretory response, at an infinitely high calcium level) and KmCa (the calcium concentration yielding half-maximal secretion). Neither addition of eserine, to indirectly activate muscarinic autoinhibition, nor of atropine to block it, markedly affected VmaxCa. In the absence of these drugs KmCa was about 3.5 mM. Eserine raised it about 7-fold, while further addition of atropine reversed this effect. The competitive pattern of interaction of drugs altering muscarinic autoinhibition, with the calcium dependence of the secretory mechanisms, suggest that this control is exerted by restriction of the ability of the nerve terminals to utilize external calcium.

Acetylcholine↗

PubMed2003

Involvement of protein kinase C in the adaptive changes of cholinergic neurons to sympathetic denervation in the guinea pig myenteric plexus.

Supersensitivity to muscarinic, kappa- and mu-opioid agents modulating cholinergic neurons in the guinea pig colon develops after chronic sympathetic denervation. A possible role for protein kinase C (PKC) in contributing to development of these sensitivity changes was investigated. The PKC activator, phorbol-12-myristate-13-acetate (PMA), enhanced acetylcholine (ACh) overflow in preparations obtained from normal animals. The facilitatory effect of PMA was significantly reduced after prolonged exposure to the phorbol ester and by the PKC inhibitors, chelerythrine and calphostin C. Subsensitivity to the facilitatory effect of PMA developed after chronic sympathetic denervation. In this experimental condition, immunoblot analysis revealed reduced levels of PKC in myenteric plexus synaptosomes. The facilitatory effect of the muscarininc antagonist, scopolamine, on ACh overflow was significantly reduced by the phospolipase C (PLC) inhibitor, U73122, chelerythrine and calphostin C, both in normal and denervated animals. However, in both experimental groups, PLC antagonists and PKC antagonists did not affect the inhibitory effect of the muscarinic agonist, oxotremorine-M on ACh overflow. The inhibitory effects of U69593 (kappa-opioid receptor agonist) and DAMGO (mu-opioid receptor agonist) on ACh overflow significantly increased in the presence of U73122, chelerythrine and calphostin C in preparations obtained from normal animals, but not in those obtained from sympathetically denervated animals. These results indicate that activation of PKC enhances ACh release in the myenteric plexus of the guinea pig colon. At this level, chronic sympathetic denervation entails a reduced efficiency of the enzyme. In addition, PKC is involved in the inhibitory modulation of ACh release mediated by muscarinic-, kappa- and mu-opioid receptors, although with different modalities. Muscarinic receptors inhibit PKC activity, whereas kappa- and mu-opioid receptors increase PKC activity. Both the inhibitory and the facilitatory effect on PKC involve modulation of PLC activity. The possibility that the change in PKC activity represents one of the biochemical mechanisms at the basis of development of sensitivity changes to opioid and muscarinic agents after chronic sympathetic denervation is discussed.

Acetylcholine↗

PubMed1989

Spread of herpes simplex virus type-1 (Miyama +GC strain) to the central nervous system after intraperitoneal inoculation: the role of the myenteric plexus of the gut.

The pathways taken by the HSV-1 virus after intraperitoneal (i.p.) inoculation were studied in 5-week old male C3H/HeN mice injected with 1 x 10(4) PFU (100 LD50) or 5 x 10(5) PFU (5000 LD50) of HSV-1 (Miyama +GC strain). At the higher dosage (5 x 10(5) PFU), HSV-1 began replicating in the adrenal from the first day, then in the gut and thoracic portion of the spinal cord by the third day, and in the brainstem by the fourth day, as shown by the titers of the virus in these organs. By immunoperoxidase staining HSV-1 was localized in a necrotic area of the adrenal, the myenteric plexus of the gut, the intermediolateral columns of the thoracic cord, and the vagus nerve nuclei of the medulla oblongata. In the low dose mice (1 x 10(4) PFU), HSV-1 was not isolated from the adrenal or thoracic segment of the spinal cord from the time of inoculation until the time of death. It was, however, isolated from the gut on days 4-6 and from the brainstem by day 5. HSV-1 was never isolated from the blood of either group at any time. The localizations of viral replication suggest that in the mice inoculated with 1 x 10(4) PFU, HSV-1 spreads to the brainstem via the vagal nerves after replication in the myenteric plexus of the gut. In the mice given the higher dose, localizations suggest not only the above route, but also that the virus spread to the intermediolateral columns of the spinal cord after replicating in the adrenal.

Animals↗

PubMed2003

Long vasodilator reflexes projecting through the myenteric plexus in guinea-pig ileum.

This study examined enteric neural reflexes activating submucosal cholinergic vasodilator motoneurons, which innervate the final resistance vessels regulating mucosal blood flow. Videomicroscopy was employed to monitor dilatation of submucosal arterioles in in vitro preparations from guinea-pig ileum. Balloon distension of intact lumen evoked reflex vasodilatation and flat sheet preparations were employed to separate mucosal mechanical stimulation from intestinal distension. Mucosal stroking and balloon distension of the orad segment evoked vasodilatations > 1.5 cm from the stimulating site. Mucosal stimulation was blocked by combined 5-HT3/5HT4 antagonists but distension-evoked responses were unaffected. Distension-evoked responses were also unaffected by nifedipine (5 microM) or nifedipine (1 microM) and wortmannin (300 nM), suggesting stretch activation rather than stretch-activated contraction was involved. Mucosal and distension-evoked responses were completely blocked when the myenteric plexus was surgically lesioned and were significantly inhibited by hexamethonium. The muscarinic antagonist 4-DAMP, which inhibits vasodilatations evoked by submucosal cholinergic vasodilator neurons, blocked dilatations elicited by mucosal stimulation and balloon distension. Maximal dilatations evoked with either sensory modality could be further enhanced when stimulated with the second modality. Dilatations evoked by stimulation of the aborad segment were similar to those elicited in the orad segment. In conclusion, sensory mechanisms in the mucosa and muscularis propria activate vasodilator pathways in the myenteric plexus which project for significant distances in both ascending and descending directions before innervating submucosal arterioles. These reflexes could co-ordinate mucosal blood flow during multiple motor events such as peristalsis and intestinal mixing between propulsive events.

Androstadienes↗

PubMed1992

Human pancreatic polypeptide, neuropeptide Y and peptide YY reduce the contractile motility by depressing the release of acetylcholine from the myenteric plexus of the guinea pig ileum.

Transmural stimulation (TS; 15 V, 0.5 msec, 1-5 Hz, for 30 sec) caused a contraction in a frequency-dependent manner of the longitudinal muscle with myenteric plexus of the guinea pig ileum. Two-min premedication with human pancreatic polypeptide (HPP, 10(-8) M-10(-6) M), neuropeptide Y (NPY, 10(-8) M-10(-6) M), and peptide YY (PYY, 10(-8) M-10(-6) M) partially, by less than 35%, reduced TS (15 V, 0.5 msec, 10 Hz)-evoked contraction in a dose-dependent manner without affecting the resting tensions. Hexamethonium, phentolamine, prazocine, yohimbine, propranolol, naloxone and theophylline had no effects on the inhibitory actions of these peptides on TS-evoked contractions. TS (15 V, 0.5 msec, 10 Hz)-evoked 3H-ACh release was significantly reduced by 2-min premedication of HPP (10(-6) M), NPY (10(-6) M) and PYY (10(-6) M). The order of potency of these depressant effects on TS-evoked contraction and 3H-ACh release was PYY greater than NPY greater than HPP. It is suggested that the members of PP family have inhibitory effects on the contractile motility by depressing ACh release from myenteric plexus of the guinea pig ileum.

Acetylcholine↗

PubMed1998

NADPH diaphorase-containing nerve fibers and neurons in the myenteric plexus are resistant to postmortem changes: studies in Hirschsprung's disease and normal autopsy material.

OBJECTIVE: Nitric oxide is considered to be the most important messenger of inhibitory nonadrenergic, noncholinergic nerves in the enteric nervous system. Histochemical studies have shown that nitric oxide synthase is identical to reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase. Histochemical staining with NADPH diaphorase has been widely used to study nitrergic innervation of the gastrointestinal tract, but fresh tissue is considered a prerequisite for satisfactory results. The purposes of this study were to evaluate whether whole-mount specimens of human bowel obtained after death are suitable for histochemical staining with NADPH diaphorase and to compare the staining properties with those of specimens of resected bowel from patients with Hirschsprung's disease METHODS: Whole-mount preparations of the myenteric plexus were examined using NADPH diaphorase histochemical staining of bowel specimens obtained at autopsy from 18 pediatric subjects (31 specimens). Fresh tissue was also obtained from the colon of four patients with Hirschsprung's disease. The staining properties of postmortem specimens were assessed in relation to the postmortem time before fixation (<12 hours, 13-24 hours, or 25-48 hours) and were compared with those of specimens of ganglionic bowel from patients with Hirschsprung's disease. Specimens of aganglionic bowel were also stained and examined. RESULTS: Strong NADPH diaphorase staining was achieved in 26 of the 31 postmortem bowel specimens, including all specimens from patients who underwent autopsy 25 to 48 hours after death. Staining properties were similar to those obtained in ganglionic bowel specimens from patients with Hirschsprung's disease. In aganglionic bowel the normal myenteric plexus meshwork was absent and was replaced by weakly staining nerve fibers. CONCLUSION: Histochemical staining with NADPH diaphorase is a robust technique suitable for use with whole-mount preparations to demonstrate nitrergic innervation in motility disorders such as Hirshsprung's disease. The technique may be used with both fresh tissue and specimens obtained up to 48 hours after death.

Child↗

PubMed1995

Ultrastructural studies of the myenteric plexus and smooth muscle in organotypic cultures of the guinea-pig small intestine.

External muscle and myenteric plexus from the small intestine of adult guinea-pigs were maintained in vitro for 3 or 6 days. Myenteric neurons and smooth muscle cells from such organotypic cultures were examined at the electron-microscopic level. An intact basal lamina was found around the myenteric ganglia and internodal strands. Neuronal membranes, nuclei and subcellular organelles appeared to be well preserved in cultured tissues and ribosomes were abundant. Dogiel type-II neurons were distinguishable by their elongated electron-dense mitochondria, numerous lysosomes and high densities of ribosomes. Vesiculated nerve profiles contained combinations of differently shaped vesicles. Synaptic membrane specializations were found between vesiculated nerve profiles and nerve processes and cell bodies. The majority of nerve fibres were well preserved in the myenteric ganglia, in internodal strands and in bundles running between circular muscle cells. No detectable changes were found in the ultrastructure of the somata and processes of glial cells. Longitudinal and circular muscle cells from cultured tissue had clearly defined membranes with some close associations with neighbouring muscle cells. Caveolae occurred in rows that ran parallel to the long axis of the muscle cells. These results indicate that the ultrastructural features of enteric neurons and smooth muscle of the guinea-pig small intestine are well preserved in organotypic culture.

Animals↗

PubMed1969

Obstruction of bowel due to lesion in the myenteric plexus.

Two patients are described who were found to have a destructive lesion of the myenteric plexus. In one the upper small intestine was involved and the clinical picture was of recurrent pseudo-obstruction; in the other the lesion was in the distal colon and resulted in intractable constipation. The lesion cannot be demonstrated by conventional histological techniques, being seen only in silver preparations cut parallel to the bowel wall, and may have been overlooked in the past. The aetiology is unknown.

Adult↗

PubMed1988

Visualization of non-synaptic release sites in the myenteric plexus of the snail Helix pomatia.

Following conventional glutaraldehyde-osmium tetroxide fixation, a rich myenteric plexus was detected in the gastrointestinal tract of the snail Helix pomatia. Although hundreds of nerve processes were observed in the extensive myoneural neuropil, true synaptic specializations were not recognized in them. In the absence of synaptic specializations, tannic acid-Ringer incubation was applied to visualize the non-synaptic release sites in the enteric nerve plexus. After incubation for 1 h, a great number of exocytosis profiles were recorded at nerve-muscle contacts, at axoglial connections and in the myoneural neuropil. The frequency of occurrence of exocytosis profiles was the same for adrenergic and peptidergic fibres. In some gut wall areas, a dense staining of both basal lamina and collagen fibres was observed. Invagination of dense basal lamina into the omega-shaped profiles of the axolemma led to "false exocytosis" profiles. A detailed morphological analysis is needed to distinguish false exocytosis profiles from the true transmitter-releasing loci.

Animals↗

PubMed1991

Ramifications of the axons of AH-neurons injected with the intracellular marker biocytin in the myenteric plexus of the guinea pig small intestine.

The projections and terminal ramifications of electrophysiologically characterized myenteric neurons of the guinea pig small intestine were studied after intracellular injection of the marker substance biocytin. Myenteric neurons were impaled with microelectrodes containing 4% biocytin in 2 M KCl (pH 7.4) and characterized electrophysiologically as either AH-neurons or S-neurons. AH-neurons were neurons in which action potentials were followed by prolonged after-hyperpolarizations (lasting greater than 4 seconds). S-neurons were neurons in which such hyperpolarizations were not seen. Electrical stimulation of internodal strands evoked prominent fast excitatory synaptic potentials in S-neurons, but not in AH-neurons. Biocytin was injected electrophoretically into the impaled AH-neurons by passage of hyperpolarizing current (0.6-0.8 nA for 5-15 minutes) through the recording electrode. The preparation was then fixed in Zamboni's fixative, dehydrated, and exposed to avidin coupled to horseradish peroxidase which allowed the injected biocytin to be visualised via a diaminobenzidine reaction. In many cases, the injected biocytin appeared to fill all the processes of injected AH-neurons that ramified within the myenteric plexus. The filled processes included axons running up to 4 mm within the plexus and profuse varicose terminals ramifying within both the ganglion containing the injected cell body and nearby ganglia. Most (90%) cell bodies of the injected AH-neurons had the morphology of Dogiel type II neurons; large, mostly smooth cell bodies with few short processes and several long processes. The other 10% of the AH-neurons had similar cell bodies and long processes but also had prominent short filamentous processes. This population was termed dendritic AH-neurons. The projections and terminals of 28 AH/Dogiel type II neurons and 7 dendritic AH-neurons were analysed in detail. Both types of neurons project circumferentially to provide terminals to nearby ganglia, but the AH/Dogiel type II neurons also provide terminals to their own ganglia while the dendritic AH-neurons typically do not. Although many of the injected AH-neurons had projections orally or anally along the intestine no evidence for a preferential direction of projection was obtained. Analysis of the areas and distributions of the terminal fields of the AH/Dogiel type II neurons suggests that each may contact several other myenteric neurons and that each myenteric neuron may receive input from about ten AH/Dogiel type II neurons.

Action Potentials↗

PubMed1995

Differential projection of cholinergic and nitroxidergic neurons in the myenteric plexus of guinea pig stomach.

The aim of this study was to investigate the organization of myenteric circuits in the guinea pig stomach. Intracellular neurobiotin injections followed by choline acetyltransferase (ChAT) immunohistochemistry and NADPH-diaphorase reaction were used to identify projections of cholinergic and nitroxidergic neurons. Neurons were classified as motor neurons based on varicose endings in the muscle or the occurrence of retraction bulbs, as nonmotor neurons if varicose endings terminated onto other ganglion cells, or as multitargeted neurons. ChAT-positive cells are composed of 64% motor, 27% nonmotor, and 9% multitargeted neurons. The percentages for NADPH-reactive motor, nonmotor, and multitargeted neurons were 57, 39, and 4%, respectively. The majority of ChAT-positive motor (81%) and nonmotor neurons (85%) had ascending projections. In contrast, the majority of NADPH-reactive motor (86%) and nonmotor neurons (86%) had descending projections. Cell bodies of ascending neurons were smaller in size than the descending neurons. The results indicate that ChAT- and NADPH-neurons in the stomach have preferred projections, the former being primarily ascending, the latter mainly descending neurons. This suggests the existence of a basic circuit for polarized reflexes in the myenteric plexus of the stomach, which might mediate descending relaxation and ascending excitation.

Amino Acid Oxidoreductases↗

PubMed1986

Effects of exposure to high potassium concentration on the longitudinal muscle-myenteric plexus preparation from guinea-pig.

The effect of potassium on the longitudinal muscle-myenteric plexus (LM-MP) preparation from guinea-pig was studied. The strips were exposed to elevated K+ (30 mM, 60 mM, 90 mM, 120 mM or 150 mM). A phasic contraction of the LM-MP was caused by 10 mM K+ or 15 mM K+ followed by an increase of the contractile activity probably due to the increase in acetylcholine release. A higher molarity of K+ produces more marked depolarization in the LM-MP and above 22 mM K+ tetanizing effects were observed. We attempted to demonstrate that opiate-like material could be released when the tissue was exposed to more than 30 mM K+ even though several different neurotransmitters could be liberated by elevated K+ molarities.

Animals↗

PubMed1999

Analysis of fast synaptic pathways in myenteric plexus of guinea pig ileum.

Most fast excitatory postsynaptic potentials (fEPSPs) recorded from guinea pig ileum myenteric plexus are mediated by acetylcholine acting at nicotinic receptors and ATP acting at P2X receptors. These studies examine length and polarity of projection of neurons releasing mediators of fEPSPs. Under ketamine-xylazine anesthesia, animals were sham treated or myenteric pathways were interrupted. After severed axons degenerated, fEPSPs were recorded at the operated site using conventional, intracellular electrophysiological methods and were classified as nicotinic or mixed on the basis of sensitivity to hexamethonium. Cholinergic and noncholinergic fEPSPs were recorded from small, operated segments, suggesting that some neurons have projections between adjacent ganglia. The mean amplitudes of nicotinic and mixed fEPSPs were reduced after circumferential and descending pathways degenerated. The proportion of nicotinic vs. mixed fEPSPs recorded from tissues lacking descending projections was greater than that recorded from sham-treated tissues, suggesting that fibers releasing noncholinergic mediators project aborally. Descending projections communicate with neurons in ganglia at least three rows aboral to their origin. The data suggest that fast noncholinergic neurotransmission could contribute to hexamethonium-resistant descending inhibition during the peristaltic reflex.

Animals↗

PubMed1976

Storage and release of labelled acetylcholine in the myenteric plexus of the guinea-pig ileum.

Guinea-pig ileum myenteric plexus-longitudinal muscle preparation was superfused with [3H]choline for 15 min either without being stimulated or during field stimulation at 0.1 or 16 Hz; the preparation was then either removed immediately or after 75- or 135-min superfusion with hemicholinium-3 (HC-3) and the total acetylcholine (ACh) and [3H]ACh contents were determined. For measuring the release of [3H]ACh the preparation was stimulated for 60 min the second time at 0.1 or 16 HZ in the presence of hemicholinium. Exposure to [3H]choline without stimulation resulted in the formation of [3H]ACh stores which were maintained in the first 75 min but decreased therafter. Labelling during stimulation at 16 Hz produced the largest and best maintained [3H]ACh content. Following labelling during 0.1-Hz stimulation, more label could be released than following labelling in the absence of stimulation. Labelling during 16-Hz stimulation did not increase any further in fool of [3H]ACh accessible to release by 0.1-Hz stimulation, but caused a 2.5 times increase in the pool from which Hz stimulation released [3H]ACh. These results suggest that two populations of cholinergic neurons exist in the myenteric plexus, one activated only by high frequency stimulation, the other by both high and low frequency stimulation.

Acetylcholine↗

PubMed1973

The calcium-dependent slow after-hyperpolarization in myenteric plexus neurones with tetrodotoxin-resistant action potentials.

Intracellular recordings were made from neurones of the myenteric plexus of the guinea-pig ileum. The slow after-hyperpolarization which followed an action potential in some neurones was abolished by Mn(++), La(+++) and by solutions which contained no Ca(++). In these neurones, the action potential and the slow after-hyperpolarization persisted in Na(+)-free solutions or in the presence of tetrodotoxin (2 muM). The findings suggest that an inward Ca(++) current during the action potential is essential for the slow after-hyperpolarization.

Action Potentials↗