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At least 19 recordsLinked to original sources
PubMed1990

The topographical basis of cholinergic transmission in guinea-pig ileum myenteric plexus.

Myenteric plexus-longitudinal muscle strips were used to study nerve action potential propagation and transmission and their differences between the proximal and the distal regions of cholinergic terminals. Neurogenic twitches of a portion of the strip were evoked by focal electrical stimulation. Twitches mediated by the distal regions of cholinergic nerve terminals were more influenced by drugs affecting Ca2+ "utilization" (Bay K 8644, kappa opiate ligand ethylketocyclazocine, changes in extracellular Ca2+ or Co2+ concentration) in contrast to twitches mediated by proximal regions of these terminals which were more influenced by drugs affecting sodium-potassium spike (tetrodotoxin, dendrotoxin, 4-aminopyridine, tetraethylammonium). Post-tetanic potentiation of twitches was prominent with that portion of the strip where the distal regions of nerve terminals were involved. Drugs interfering with Na+/K+ spikes indiscriminately influenced both the twitch height and post-tetanic potentiation whereas changes in extracellular Ca2+ concentration affected selectively only post-tetanic potentiation. Release of [3H]acetylcholine from pre-labelled strips evoked by 1 Hz continuous stimulation or by train stimulation at 30 Hz was measured selectively from portions containing either proximal and distal or only distal regions of nerve terminals. The release from portions containing the distal regions was relatively higher when evoked by 30 Hz than by 1 Hz. The distal regions of nerve terminals might be thus recruited to participate in transmission by a frequency-dependent process. Nerve impulses were recorded from strands of nerve fibres in the myenteric plexus. At 1 and 5 mm distance from the stimulation focus nerve impulses were completely suppressed by tetrodotoxin. At 5 mm, in some strands the amplitude of nerve impulses was also subject to the effect of drugs affecting Ca2+ "utilization"; facilitation of nerve impulse amplitude during 30 Hz train stimulation was always influenced by drugs affecting Ca2+ "utilization". Propagation of nerve impulses in the distal region of cholinergic nerve terminals was found to be Ca-sensitive and frequency-dependent; this might form the basis for facilitation and post-tetanic potentiation of muscarinic transmission.

Acetylcholine↗
PubMed1977

[Functional organization of the ganglia of the myenteric plexus].

In myenteral plexus of isolated segments of the small intestine and colon, presence of spontaneously active and silent cells was shown. The former discharge in separate action potentials with variable interval or in periodic bursts with relatively long intervals in between. The silent cells have a major group of mechanosensitive neurons and the neurons responding to pharmacological agents or to biologically active substances. The simplest interneuronal relations are considered in the myenteral ganglion: the excitatory and inhibitory connections, signs of organization in the neuronal activity. On the basis of own and literature data, a hypothetical scheme of functional organization of the myenteral plexus' ganglions is suggested.

Adaptation, Physiological↗
PubMed1990

Neuropeptide release from isolated myenteric nerve endings derived from the guinea pig myenteric plexus.

Isolated myenteric nerve varicosities prepared from the myenteric plexus of the guinea pig ileum were investigated as a suitable model system with which to study the release of several neuropeptide-like immunoreactivities (-LI). Basal release of substance P-LI, neurokinin A-LI, Leu-enkephalin-LI and Met-enkephalin-LI was determined, and clear depolarization-induced release of the enkephalin-LI's and neurokinin A-LI was obtained using this preparation, providing further support for their roles as putative mediators in the enteric nervous system. Evoked-release of these peptides was dependent on the presence in the incubation mixture of certain antagonists to known endogenous neuronal mediators. In the absence of such antagonists, no unequivocal evidence of release was seen. Clear evoked release of Leu-enkephalin-LI occurred only in the presence of the adenosine receptor antagonist 1,3-dipropyl-8-p-sulfophenylxanthine (DPSPX), atropine and naloxone. Release of Met-enkephalin-LI occurred in the presence of either atropine or naloxone. The release of neurokinin A-LI was evident in the presence of DPSPX. These findings suggest the existence of either distinct subpopulations of nerve varicosities or distinct neuronal pools containing each peptide and that these peptides may be under differential regulation by endogenous inhibitory mediators. It is concluded that, under suitable conditions, isolated myenteric nerve varicosities provide a useful model system for the study of release, and the modulation of release, of endogenous neuropeptides.

Animals↗
PubMed1991

The innervation of the gastrointestinal tract of a chelonian reptile, Pseudemys scripta elegans. II. Distribution of neuropeptides in the myenteric plexus.

The myenteric plexus of the stomach, midgut and hindgut of the red-eared turtle, Pseudemys scripta elegans, has been investigated for the occurrence of immunoreactivity to nine neuropeptides. Neuropeptide Y (NPY)-, calcitonin gene-related peptide (CGRP)-, bombesin (BOM)- as well as substance P (SP)-like immunoreactivity (LI) were found in nerve fibres of all investigated gut regions. From all peptides investigated immunoreactivity for NPY was more pronounced. In the stomach NPY-LI was mainly found in the perikarya, while in the midgut region both NPY-immunoreactive (IR) somata and nerve fibres were revealed. The hindgut harboured few NPY-IR nerve cells and nerve fibres. A few SP-IR nerve cell bodies were observed in the stomach and midgut region. In the hindgut BOM-IR neuronal cell bodies were found. Neuromedin U (NMU)-LI was mainly observed in the stomach region, revealing both immunoreactive perikarya and nerve fibres. Immunoreactivity for vasoactive intestinal polypeptide, somatostatin, galanin and enkephalin could not be detected so far. Double labelling experiments revealed the coexistence of CGRP and SP in some nerve fibres in all three gut regions examined. Some SP-IR fibres in the midgut were immunoreactive for NMU.

Animals↗
PubMed2000

Independent endocytosis of the NK(1) and NK(3) tachykinin receptors in neurons of the rat myenteric plexus.

In the myenteric plexus of rat ileum, NK(1) and NK(3) receptors are co-located almost exclusively on neurons of a single population. This study compares endocytosis of NK(1) and NK(3) receptors in these neurons. In the absence of agonist, 26.2+/-2.8% of NK(1) receptor and 29.1+/-1.1% of NK(3) receptor was located in the cytoplasm of the neurons; the remaining receptor was on the surface. The tachykinin neurotransmitters, substance P (10 pM-10 microM) and neurokinin A (10 pM-100 microM), both induced concentration-dependent endocytosis of NK(1) and NK(3) receptors. The selective NK(1) receptor agonist, [Sar(9),Met(O(2))(11)]-substance P (1 microM), induced endocytosis of NK(1) receptor (64.2+/-1.5% in cytoplasm) but not NK(3) receptor (32.9+/-5.0%). The NK(1) receptor endocytosis was reduced by the selective NK(1) receptor antagonist, CP-99994 (100 nM), but not by the selective NK(3) receptor antagonist, SR-142801 (1 microM). The selective NK(3) receptor agonist, senktide (10 nM), induced endocytosis of NK(3) receptor (61.2+/-5.4%) but not NK(1) receptor (34.0+/-4.5%). The NK(3) receptor endocytosis was blocked by SR-142801 but not by CP-99994. We also investigated the effects of monensin, which generally blocks recycling of endocytosed receptor. In the absence or presence of exogenous agonist, monensin caused a build-up of NK(1) receptor, but not NK(3) receptor, in the cytoplasm of neurons.The results demonstrate independent, agonist-induced endocytosis of NK(1) and NK(3) receptors in neurons of the myenteric plexus of rat ileum and suggest that the mechanisms of recycling of NK(1) and NK(3) receptors differ.

Animals↗
PubMed1994

Charybdotoxin and iberiotoxin but not apamin abolish the slow after-hyperpolarization in myenteric plexus neurons.

Myenteric neurons of guinea-pig ileum were studied with intracellular microelectrodes. The specific toxins charybdotoxin, iberiotoxin and apamin were used to characterize the prolonged after-hyperpolarizations of AH neurons in this preparation. Charybdotoxin and iberiotoxin blocked prolonged after-hyperpolarizations in 23 of 24 AH neurons, but apamin had no effect on 5 of 5 AH neurons. Abolition of the after-hyperpolarizations was accompanied by depolarization and increases in input resistances of those AH neurons affected, but the shapes of action potentials were unchanged. The excitability of the AH neurons was enhanced as shown by an increase in the number of action potentials evoked by a 500-ms depolarizing current pulse or by a train of 15-ms depolarizing current pulses (10Hz). The other class of myenteric neurons, S neurons, was also investigated. The 19 S neurons studied fired action potentials only at the start of a 500 ms depolarization, but the toxins had no effect on this behaviour or on their other properties. Intracellular injection of Neurobiotin into the neurons studied and subsequent immunohistochemical staining to localise the calcium-binding protein, calretinin, indicated that all major classes of S neurons were included in the sample. Thus, the prolonged after-hyperpolarizations in AH neurons may be due to opening of a large-conductance (BK) calcium-dependent potassium channel, but similar channels play little or no role in regulation of the excitability of S neurons.

Animals↗
PubMed1976

Ultrastructural study of nerve terminals in the submucous plexus and mucous membrane after extirpation of the myenteric plexus.

An attempt is made to separate in the submucous plexus and mucous membrane of the chronically isolated intestine of the cat the fibers originating from the myenteric plexus and those originating from the submucous plexus by secondary degeneration after the extirpation of the myenteric plexus. A considerable part of the nerve processes in the submucous plexus originate from the cells of the myenteric ganglia and establish direct synaptic relationships between the ganglion cells, or are very close to the blood vessels. The numerous intact synapses between the different nerve elements in the submucous plexus point to local reflex connexions within the plexus itself. The degeneration of sub-epithelial nerve elements, containing always clear and dense-core (1,000-1,200 A in diameter) vesicles besides the numerous intact nerve elements, might indicate the presence of real sensory nerve processes in this layer. The terminal fibers remaining intact after removal of the myenteric plexus contain numerous medium-sized dense-core vesicles in potassium permanganate-fixed material. This suggests that there are cells containing 5-hydroxytryptamine in the submucous plexus.

Animals↗
PubMed1995

Tyrosine hydroxylase-containing fibres extend from the rat corpus striatum into grafts of muscularis externa and myenteric plexus.

Intrastriatal grafts of myenteric plexus produce a vigorous sprouting response in the surrounding rat brain. Since the striatum receives profuse dopaminergic innervation from the substantia nigra, we have investigated whether central catecholaminergic neurons participated in the sprouting response and grew into grafts of adult myenteric plexus (surrounded by smooth muscle) implanted in the adult corpus striatum. Three weeks after implantation, tyrosine hydroxylase-containing fibres were observed to have grown into, and ramified within, the grafts. The extent of innervation was increased 6 weeks after implantation, and was not diminished if the superior cervical ganglia were removed (to destroy any fibres of sympathetic origin).

Age Factors↗
PubMedDate not supplied

Neurological disorders of the myenteric plexus: a review.

The myenteric plexus is the neuronal complex that regulates the motility of the gut; a brief review of its pathology is presented in this paper as well as a tentative etiopathogenetic classification. Disorders of gut innervation include congenital (e.g. Hirschsprung's disease) or acquired diseases; the latter can be idiopathic or related to a more general pathological involvement of the whole organism as in the case of bacterial toxins, diabetes mellitus, Riley-Day disease and primary orthostatic hypotension. In view of the fundamental similarity of the myenteric plexus to the central nervous system, the study of this organ can be useful both for diagnosis of degenerative diseases of the central nervous system (i.e. via rectal biopsy) and for gaining a better etiopathogenetic insight into peripheral and central nervous system disease.

Alcoholism↗
PubMed1989

Somatostatin release from isolated ganglia of the myenteric plexus.

Somatostatin neurons of the myenteric plexus project caudad exclusively within the plexus synapsing with neurons in the same or other ganglia. Isolated ganglia offer a unique opportunity to examine peptide transmitter release from these interneurons. Ganglia were isolated from the myenteric plexus by sequential enzymatic digestion, centrifugation, and filtration. Single ganglia were harvested by suction and dispersed in polyacrylamide gel. The ganglia were placed in chambers (200 ganglia/chamber) and perfused with Krebs medium at the rate of 1 ml/min. Addition of the nicotinic agonist, dimethylphenylpiperazinium (DMPP), caused a concomitant increase in somatostatin (152%; P less than 0.001) and vasoactive intestinal peptide (VIP) (79%; P less than 0.05) release above basal level that was abolished by hexamethonium. Addition of the VIP antagonist, VIP-(10-28), (5 microM), to the perfusate augmented significantly DMPP-induced somatostatin release (440%; P less than 0.05), implying that the concomitant release of VIP attenuates somatostatin release. Addition of VIP (1 microM) to the perfusate abolished somatostatin release, confirming the ability of VIP to inhibit somatostatin release. The study shows that VIP interneurons exert a regulatory feedback control over somatostatin interneurons in the myenteric plexus.

Animals↗
PubMed2001

Isolation of enteric glia and establishment of transformed enteroglial cell lines from the myenteric plexus of adult rat.

Although enteroglial cells (EGCs) may play a key role in the inflammatory response of the enteric nervous system, little is known about their immunophysiological properties. To facilitate further characterization of enteric glia, we have developed a novel method to isolate and purify EGCs from the myenteric plexus. Myenteric plexus preparations were enzymatically dissociated and EGCs purified by complement-mediated cytolysis of contaminating cells and transformed by retroviral gene transfer. Primary and transformed cells were characterized immunohistochemically and by dot-blot analysis. Functionally, c-fos mRNA expression was assessed in primary and transformed enteroglial cells. All cells displayed robust glial fibrillary acidic protein, S-100 and vimentin immunoreactivities, but no Thy-1.1, desmin, smooth muscle alpha-actin or C3 complement receptor immunoreactivity. This confirmed their enteroglial lineage and excluded contamination with other cell types. Both primary and transformed EGCs displayed little constitutive c-fos mRNA expression. This, however, could be upregulated by various stimuli, including proinflammatory cytokines. In summary, we present a novel method to purify EGCs from rat myenteric plexus for tissue culture and to establish transformed EGC lines that retain their glial nature and functional properties. Such cell lines are now available for physiological studies of the functional properties of enteric glia in vitro.

Animals↗
PubMed1990

Pharmacologic characterization of the changes in cholinergic sensitivity of rat jejunal circular muscle after myenteric plexus ablation.

Neurons located in the myenteric plexus are generally believed responsible for motor control of intestinal circular muscle. The in vitro isometric responses of naive and myenterically denervated (MD) rat jejunal circular muscle to bethanechol and carbachol, alone and in the presence and absence of neuronal antagonists (hexamethonium bromide, tetrodotoxin and Botulinum toxin A) 15 and 30 days after myenteric plexus ablation, were determined. The responses to bethanechol indicated no differences in muscarinic sensitivity between naive and MD tissue. The relative potency of carbachol, which acts at both muscarinic and nicotinic receptors, in MD tissue 15 days after denervation was significantly higher than that in naive tissue. However, 30 days after denervation, the relative potencies of carbachol in naive and MD circular muscle were comparable. The presence of neuronal antagonists had no effect on the relative potency of carbachol 15 days after myenteric denervation, but altered significantly the responses 30 days after denervation. The effects produced by the neuronal antagonists 30 days after myenteric denervation were qualitatively and quantitatively different than those produced in naive tissue, suggesting that the nature of the innervation in these tissues was different. These results demonstrate that circular muscle was denervated initially after myenteric plexus ablation but reinnervation occurred within 30 days. The reinnervation observed is likely due to neurons located in the submucosal plexus.

Animals↗
PubMed1997

A new method for the isolation of myenteric plexus from the newborn rat gastrointestinal tract.

The myenteric plexus is not only essential for gastrointestinal functions, but it is also a very interesting model for the study of neuronal circuits and neuron-glial interrelationships and may be a valuable source of donor tissue, for grafting into different regions of the central nervous system. For both grafting and culture procedures it is a great advantage to obtain the maximum amount of tissue. To date, most studies have isolated the myenteric plexus by manual microdissection after collagenase digestion. Using this method, it has only been possible to obtain relatively small amounts of the myenteric plexus, mostly from the cecum and proximal colon of the guinea-pig or rat. We present here a new method, which enables much greater quantities of the plexus from the small intestine and colon to be obtained. The myenteric plexus of the entire small intestine can be isolated by a combination of enzymatic digestion and mechanical agitation. The method works from birth up to 3 week old pups, and with some modifications tissue from older or even adult animals can also be processed. Another advantage over the microdissection method is that the myenteric plexuses of the different parts of the intestine can be cultured and studied separately.

Animals↗
PubMed1991

Interaction of ethanol and L-glutamate in the guinea pig ileum myenteric plexus.

The guinea pig ileum longitudinal muscle myenteric plexus has recently been shown to contain receptors for excitatory amino acids like L-glutamate which are pharmacologically similar to the N-methyl-D-aspartate (NMDA) receptor subtype in the central nervous system (CNS). The present study utilized the longitudinal muscle myenteric plexus preparation to determine whether the reported ability of acute ethanol treatment to inhibit NMDA receptor activation in mammalian CNS preparations also occurs in the periphery. In the absence of Mg2+, L-glutamate (3-100 microM) induced transient contractions in longitudinal muscle myenteric plexus that could be blocked by atropine. Contractile responses to L-glutamate were completely blocked by D,L-2-amino-5-phosphonovalerate (APV; 100 microM) and Mg2+ (600 microM). Preincubation with ethanol (30-100 mM) for 2 min inhibited contractions to L-glutamate by up to 50% and caused additive inhibition with 100 microM Mg2+. Ethanol (65 mM) inhibition of L-glutamate (60 microM) contractions increased from 30% after a 2 min preincubation to a maximum of 60% following 10 min. Ethanol (65 mM) inhibited contractions induced by acetylcholine (0.1 microM), 5-hydroxytryptamine (0.1 microM) or histamine (0.3 microM), by no more than 10% suggesting that impairment of smooth muscle or cholinergic neuronal activity were not likely responsible for the 40% inhibition of L-glutamate contractions seen with ethanol. A previously identified contractile response to ethanol (10-300 mM), occurring immediately after addition to the longitudinal muscle myenteric plexus preparation, was still present in Mg2+ deficient buffer.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1998

Evidence for a neurotransmitter role of glutamate in guinea pig myenteric plexus neurons.

Longitudinal muscle-myenteric plexus strips of the guinea pig ileum were used to investigate a possible transmitter role of glutamate (Glu) in the enteric nervous system. Glu was released from this nerve muscle preparation by high K(+)-depolarization in a Ca2(+)-dependent manner, by electrical field stimulation and by the ganglionic stimulant dimethylphenylpiperazinium which indicates its neural origin. Contractions of the longitudinal muscle evoked by electrical stimulation of the myenteric nerves or by Glu, were significantly reduced by the N-methyl-D-aspartate (NMDA)-receptor antagonist FR115427 (9 and 18 microM), whereas contractions induced by histamine were unaffected. The results show that the amino acid Glu is likely to play an excitatory neurotransmitter role via NMDA receptors in the myenteric plexus of the guinea pig.

Animals↗
PubMed1985

Morphology and serotonergic innervation of physiologically identified cells of the guinea pig's myenteric plexus.

Ganglion cells of the myenteric plexus of the guinea pig were physiologically classified as to cell type using intracellular microelectrodes containing horseradish peroxidase (HRP). Interganglionic fiber tracts were then stimulated in an attempt to elicit slow excitatory postsynaptic potentials (EPSPs) in the impaled cells. The presence or absence of a slow EPSP was noted, following which the cells were injected with HRP through the recording micropipette and finally were incubated with tritiated 5-hydroxytryptamine ([3H]-5-HT; 0.5 microM) and desmethylimipramine (10 nM). The preparations were examined by light and electron microscopy (EM) for which the physiologically identified, HRP-injected neurons were demonstrated histochemically and serotonergic nerve terminals were simultaneously demonstrated radioautographically. Forty-seven cells were physiologically identified, injected with HRP, and studied by light microscopy. Of these, 22 were also fully analyzed by electron microscopy. The sample included 13 type I/S cells (6 analyzed by electron microscopic radioautography), 16 type II/AH cells (10 analyzed by electron microscopic radioautography), and 18 nonspiking (NS) cells (6 analyzed by electron microscopic radioautography). Slow EPSPs were only observed in type II/AH cells. All five of the fully analyzed subset of type II/AH cells that manifested a slow EPSP were contacted by serotonergic terminals. These terminals were found on 7 of 10 type II/AH cells, 2 of 6 type I/S cells, and 0 of 6 NS cells. Serotonergic terminals, therefore, contacted type II/AH cells (p less than 0.05) and especially those that showed a slow EPSP (p less than 0.005) more frequently than other types of ganglion cells. Morphologically, cells with short, stubby dendrites were reproducibly found to be type I/S cells, and glia could be recognized by their astrocytic appearance; however, cell shape did not otherwise correlate with physiological cell type. These data are compatible with and provide support for the hypothesis that 5-HT is one of the mediators of slow EPSPs in the myenteric plexus.

Animals↗
PubMed1996

Neurite outgrowth of striatal neurons in vitro: involvement of purines in the growth-promoting effect of myenteric plexus explants.

We have shown previously that a soluble factor(s) released by the myenteric plexus promotes neurite outgrowth from postnatal striatal neurons, and that this effect was abolished by tetrodotoxin. We have now investigated the possible involvement of purines in the mediation of this neuritogenic response, by examining their effect on neurite length of striatal neurons both in co-culture with myenteric plexus explants and cultured alone. Both ATP and 2-chloroadenosine partially reversed the inhibitory effect of tetrodotoxin in co-cultures with whole myenteric plexus, while the stable ATP analogue, alpha, beta-methylene ATP, had no effect, suggesting that ATP was being broken down to adenosine before exerting its action. Further support for this view was that the ATP (P2) purinoceptor antagonist suramin did not reverse the effects of ATP, while the adenosine (P1) purinoceptor antagonist 8-(p-sulphophenyl)theophylline did antagonize the effects of ATP in tetrodotoxin-treated co-cultures. Further, both 8-(p-sulphophenyl)theophylline and adenosine deaminase reduced the effect of the myenteric plexus on striatal neurons in the absence of tetrodotoxin, and the adenylate cyclase activator forskolin completely reversed the effect of tetrodotoxin in our co-culture system. The neurite outgrowth-promoting effect of 2-chloroadenosine in tetrodotoxin-treated co-cultures was not further enhanced by a combination of neuropeptides. Serotonin and GTP were without effect on striatal neurons in the presence or absence of myenteric plexus explants. In experiments without myenteric plexus, both 2-chloroadenosine and forskolin caused a slight increase in striatal neurite length; ATP and GTP were ineffective. Basic fibroblast growth factor, nerve growth factor, neurotrophin-3 or neurotrophin-4/5 had no effect on neurite outgrowth in postnatal striatal cultures after two days in vitro. When these growth factors were added in combination with 2-chloroadenosine, the observed increase in mean neurite length did not exceed that induced by 2-chloroadenosine alone. Both 2-chloroadenosine and the ganglioside mix AGF1 increased neurite elongation of striatal neurons after two days in vitro, but an inhibition of enhanced neurite outgrowth was observed when both substances were added together. Both laminin and fibronectin were not neuritogenic for postnatal striatal neurons under our culture conditions. These observations suggest that a factor other than the growth factors tested here is involved in the promotion of striatal neurite outgrowth in co-culture with myenteric plexus explants. In summary, adenosine (probably acting through the A2 subclass of the P1 purinoceptor) leads to increased striatal neurite outgrowth in co-culture with myenteric plexus and we propose that it does so either (1) by triggering the release of a neuritogenic factor, possibly from enteric glial cells, or (2) by acting synergistically with such a growth factor. Adenosine acts via P1 purinoceptors, which leads to changes in cyclic AMP, and the response to forskolin suggests that cyclic AMP is probably involved in the events leading to increased striatal neurite outgrowth.

2-Chloroadenosine↗