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 73 records · Page 4Linked to original sources

PubMed1998

Myenteric plexus in the gastrointestinal tract of non-obese diabetic mice.

The myenteric plexus was investigated in the gastrointestinal tract of pre-diabetic and diabetic non-obese diabetic (NOD) mice. The plexus was immunostained by the avidin-biotin complex method, using a general marker for nerve elements, namely protein gene-product 9.5. The nerve fibres were quantified by point-counting and the number of ganglia and their area were determined by image analysis. The relative volume density of the nerve fibres in duodenal muscularis propria was found to be significantly reduced in of both pre-diabetic and diabetic NOD mice. There was no statistical difference between controls and NOD mice regarding relative volume density of nerve fibres in antral and colonic muscularis propria. The number of myenteric ganglia/mm baseline was significantly decreased in the duodenum of diabetic NOD mice, and showed a non-statistically significant tendency to decrease in pre-diabetic mice. In the antrum and colon, there was no difference between the controls and NOD mice regarding the number of ganglia/mm baseline. Nor was there any significant difference between controls and NOD mice in the area of myenteric ganglia in either antrum, duodenum or colon. It is concluded that the changes in the duodenal myenteric plexus of NOD mice are prior to the onset of diabetes. It is suggested that the absence of changes in the antral and colonic myenteric plexus when using a general marker for neuroelements does not preclude a possible change in cholinergic, adrenergic or peptidergic innervation.

Animals↗

PubMed1990

Differential effects of calcium channel antagonists (omega-conotoxin GVIA, nifedipine, verapamil) on the electrically-evoked release of [3H]acetylcholine from the myenteric plexus, phrenic nerve and neocortex of rats.

Electrically-evoked release of [3H]acetylcholine from autonomic neurons (myenteric plexus), motoneurons (phrenic nerve) and the central nervous system (neocortex) was investigated in the presence and absence of the calcium channel antagonists omega-conotoxin GVIA, nifedipine and verapamil, whereby the same species (rat) was used in all experiments. Release of [3H]acetylcholine was measured after incubation of the tissue with [3H]choline. omega-Conotoxin GVIA markedly reduced (70%) the evoked release of [3H]acetylcholine from the myenteric plexus of the small intestine (IC50: 0.7 nmol/l) with a similar potency at 3 and 10 Hz stimulation. An increase in the extracellular calcium concentration attenuated the inhibitory effect of omega-conotoxin GVIA. Release of [3H]acetylcholine from the rat neocortex was also inhibited (90%) by omega-conotoxin GVIA, but the potency was 19-fold lower (IC50: 13 nmol/l). However, the release of [3H]acetylcholine from the phrenic nerve was not reduced by omega-conotoxin GVIA (100 nmol/l) at 1.8 mmol/l calcium (normal concentration), whereas omega-conotoxin GVIA inhibited evoked [3H]acetylcholine release by 47% at 0.9 mmol/l calcium. Neither nifedipine (0.1 and 1 mumol/l) nor verapamil (0.1, 1 and 10 mumol/l) modified the evoked release of [3H]acetylcholine from the myenteric plexus and the phrenic nerve. Acetylcholine release from different neurons appears to be regulated by different types of calcium channels. N-type channels play the dominant role in regulating acetylcholine release from both the myenteric plexus and the neocortex, whereas acetylcholine release from motor nerves is regulated by calcium channel(s) not yet characterized.

Acetylcholine↗

PubMed2000

Projections and neurochemistry of interneurones in the myenteric plexus of the guinea-pig gastric corpus.

Recently, motor neurones of the myenteric plexus innervating the muscle layers or the mucosa have been identified in the guinea-pig stomach. We applied the neuronal tracer DiI (1,1'-didodecyl-3,3,3', 3'-tetramethylindocarbocyanine perchlorat) onto myenteric ganglia in order to identify populations of interneurones in the myenteric plexus of the guinea-pig stomach. The tracing was combined with the immunohistochemical detection of calbindinD28k (CALB), choline acetyltransferase (ChAT), neuropeptide Y (NPY) and 5-hydroxytryptamine (serotonin) (5-HT) and the results were compared to the neurochemical coding of target specific motor neurones. Long projecting ( approximately 5.4 mm) ChAT/CALB/+/-5-HT-, nitric oxide synthase (NOS)/CALB- and short projecting ( approximately 1.1 mm) ChAT/NPY-neurones were identified as descending interneurones. CALB positive ascending interneurones contained ChAT but rarely 5-HT (code: ChAT/CALB). This study identified ascending and descending interneurones in the gastric myenteric plexus and revealed the neurochemical coding of some of the interneurone populations.

Animals↗

PubMed1998

Nicotinic receptor mediates nitric oxide synthase expression in the rat gastric myenteric plexus.

The mechanism that regulates the synthesis of nitric oxide synthase (NOS), a key enzyme responsible for NO production in the myenteric plexus, remains unknown. We investigated the roles of the vagal nerve and nicotinic synapses in the mediation of NOS synthesis in the gastric myenteric plexus in rats. Truncal vagotomy and administration of hexamethonium significantly reduced nonadrenergic, noncholinergic relaxation, the catalytic activity of NOS, the number of NOS-immunoreactive cells, and the density of NOS-immunoreactive bands and NOS mRNA bands obtained from gastric tissue. These results suggest that NOS expression in the gastric myenteric plexus is controlled by the vagal nerve and nicotinic synapses. We also investigated if stimulation of the nicotinic receptor increases neuronal NOS (nNOS) expression in cultured gastric myenteric ganglia. Incubation of cultured gastric myenteric ganglia with the nicotinic receptor agonist, 1,1-dimethyl-4-phenylpiperizinium (DMPP, 10(-10)-10(-7) M), for 24 h significantly increased the number of nNOS-immunoreactive cells and the density of immunoreactive nNOS bands and nNOS mRNA bands. nNOS mRNA expression stimulated by DMPP was antagonized by a protein kinase C antagonist, a phospholipase C inhibitor, and an intracellular Ca2+ chelator. We concluded that activation of the nicotinic receptor stimulates a Ca2+-dependent protein kinase C pathway, which in turn, upregulates nNOS mRNA expression and nNOS synthesis in the gastric myenteric plexus.

Animals↗

PubMed1985

Heterogeneity of ganglia of the guinea pig myenteric plexus: an in vitro study of the origin of terminals within single ganglia using a covalently bound fluorescent retrograde tracer.

Experiments were done to test the hypothesis that individual ganglia of the myenteric plexus of the guinea pig small intestine are heterogeneous with respect to the location of the neurons that provide terminals to them. The myenteric plexus, attached to the longitudinal layer of smooth muscle, was maintained in vitro. Individual ganglia were injected with a variety of potential retrograde tracers by pressure microejection from the tip (20-micron diameter) of a glass micropipette. The fluorescent dye 4-acetoamido, 4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS) was found to be an effective tracer, labeling neuronal perikarya, evidently by retrograde transport. SITS has previously been shown not to cross plasma membranes, but to be covalently bound to the outer surface of that membrane, and to be taken up by nerve terminals to be retrogradely transported to label neuronal cell bodies. SITS fluorescence was found in about 12% of the neurons within the ganglion into which it was injected and also in approximately ten times more neurons in discretely located distant ganglia. No labeling of neurons was found when SITS was injected into the bath or into the smooth muscle below the myenteric plexus. Damage to neural connectives obstructed the labeling of neurons in ganglia distal to the injection site. Individual SITS-injected myenteric ganglia were found to vary greatly in the ratios of intraganglionic SITS-labeled neurons to the total number of neurons within the injected ganglion. The ratios of the number of intraganglionic SITS-labeled neurons to SITS-labeled neurons in distant ganglia projecting to the injected ganglion from elsewhere in the myenteric plexus also varied greatly. More strikingly, individual ganglia differed over a wide range with respect to whether the neurons in distant ganglia that provided them with terminals were situated in the oral, anal, or circumferential direction. Although the majority of projections were found to be from orally located ganglia, individual ganglia were observed that received predominantly or exclusively anal or oral projections. Others received mixtures of terminals from ganglia that were anal, oral, or circumferential. This anatomical heterogeneity in the location of afferent inputs to individual myenteric ganglia is probably reflected in a functional heterogeneity as well and will have to be taken into account in further studies of the physiology of the myenteric plexus. Individual ganglia of the plexus can no longer be taken as anatomically and functionally equivalent to one another.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗

PubMed2003

The comparative analysis of the myenteric plexus in pigeon and hen.

Using the thiocholine method and histological techniques the myenteric plexuses of pigeon and hen were studied. Investigations revealed the presence of a nervous network in the wall of the small intestine of both animals. It consists of many nerve fibres crossing each other and creating meshes in a variety of shapes. The density of the network was different according to the species and to the parts of intestine. The myenteric plexus from the pigeon's duodenum is thicker (3.7-fold) than in the remaining part of the small intestine; in the hen this is approximately 2.2-fold thicker. The meshes of the duodenum in both species are smaller than in the jejunum and ileum. The results of histological investigations showed different localization of myenteric plexuses; in pigeon in the space between the circular and longitudinal muscle layers, and in hen within the circular muscle.

Animals↗

PubMed1997

Role of nitric oxide in norepinephrine release from myenteric plexus in vitro and in Trichinella spiralis-infected rats.

Nitric oxide (NO) has been implicated as modulator of neural function and inflammatory mediator. Previously, we have demonstrated suppression of norepinephrine (NE) release from myenteric nerves following Trichinella spiralis infection implicating interleukin-1 beta (IL-1 beta) as a mediator of these changes. In the present study, we have examined the role of NO in NE release from the myenteric plexus and in the suppression of NE release induced by IL-1 beta in vitro, and we have determined whether NO is involved in the suppression of NE release from the myenteric plexus observed in T. spiralis-infected rats. Electrically evoked NE release from jejunal longitudinal muscle-myenteric plexus preparations (LMMP) was measured following (a) in vitro exposure of the tissue to the NO donor 3-morpholinosydnonimine (SIN-1), L-arginine, or IL-1 beta, in the presence or absence of NOS inhibitors, and (b) in vivo treatment of control or T. spiralis-infected rats with N6-nitro-L-arginine-methyl-ester (L-NAME), NG-nitro-D-arginine-methyl-ester (D-NAME) or vehicle for 6 days. In vitro inhibition of NO synthesis had no effect on NE release from the myenteric plexus. Treatment with SIN-1 or L-arginine suppressed NE release in a manner similar to that observed with IL-1 beta. Moreover, the effect of IL-1 beta was attenuated by L-NAME. In contrast, treatment of T. spiralis-infected rats with L-NAME had no effect on the suppression of NE release. These results indicate that in the absence of inflammation, the myenteric plexus can generate sufficient NO to inhibit NE release and that NO mediates the action of IL-1 beta on NE release in vitro. However, we have no evidence for the involvement of NO in the suppression of NE release in nematode-infected rats.

Animals↗

PubMed1991

Synaptic connections of extrinsic nerve fibers in the myenteric plexus of the rat duodenum.

In the present study the degeneration of extrinsic nerve fibers was first investigated in the duodenal myenteric plexus after their transection, and subsequently synaptic connections of the extrinsic nerve fibers were observed with their degenerative changes to examine the relationship of the extrinsic nerve fibers with the neuronal circuits in the myenteric plexus. Adult rats were anesthetized with pentobarbital, and the extrinsic nerve fibers running with the coeliac and superior mesenteric arteries were cut at about 2 mm distance from the coeliac ganglia to duodenum. Their duodena were fixed at 6 and 12 hours, and 1, 2, 4, 7 and 11 days after the extrinsic denervation, and their myenteric plexuses were observed with the electron microscope. Then, montages on 22 fields of the myenteric plexuses of 7 days after the denervation were made, and the number of all synapses and degenerated synapses in them was counted in each montage. 1. The degenerated changes of the extrinsic nerve fibers Three types of the degenerated axons were found in stages ranging from 12 hours to 11 days after the extrinsic denervation as follows: 1) Type I appeared mainly at 1 and 2 days. The electron density in the axoplasm decreased, and the synaptic vesicles accumulated in the central area of the axoplasm. 2) Type II appeared, also, at 1 and 2 days. The electron dense material occupied the axoplasm or the myelin-like structure appeared in the slightly swollen axons. 3) Type III appeared in stages from 1 to 11 days. Electron dense bodies appeared in the axoplasm.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Ileal myenteric plexus in aged guinea-pigs: loss of structure and calretinin-immunoreactive neurones.

Myenteric plexus controls gastrointestinal motility by means of well organized circuits which are comprised of sensory neurones, interneurones and motor neurones to the muscular layers. Calretinin (CR) is a calcium-binding protein that, in guinea-pig ileum, has only been found in ascending interneurones, which also express neurofilament triplet proteins (NFT), and excitatory longitudinal muscle motor neurones, which do not. In spite of some evidence that age affects both function and structure of the myenteric plexus, little is known about the possible selectivity of the process regarding specific myenteric neuronal phenotypes. The influence of age on both the structure of the myenteric plexus and the presence of CR-immunoreactive (CR-IR) neurones was studied using conventional immunohistochemical procedures applied to ileal whole-mount preparations from guinea-pigs. Both a reduction in ganglionic size and changes in the distribution of neurones inside and outside the ganglia, together with a general neuronal loss were found in preparations from aged guinea-pigs. More interestingly, a relatively more pronounced age-related loss of CR-IR neurones, especially those lacking of NFT expression, was found. Specific myenteric neuronal phenotypes may show differential sensitivity to ageing, and this could, under certain circumstances, alter the functional balance of gastrointestinal motility in aged individuals.

Aging↗

PubMed1985

Opioid inhibition of synaptic transmission in the guinea-pig myenteric plexus.

Intracellular recordings were made from neurones in the myenteric plexus of the guinea-pig ileum. Presynaptic nerves were excited by a focal stimulating electrode on an interganglionic strand. Fast excitatory postsynaptic potentials (e.p.s.ps) were depressed in amplitude by morphine and [Met5]enkephalin in the concentration range of 1 nM-1 microM. Nicotinic depolarizations evoked by exogenously applied acetylcholine (ACh) were not affected by these opioids. Hyperpolarization of the presynaptic fibres probably contributed to the depression of the fast e.p.s.p. because fast e.p.s.ps evoked by low stimulus voltages were more depressed than those evoked by high stimulus voltages and fast e.p.s.ps resulting from activation of a single presynaptic fibre were blocked in a non-graded manner. Opioids depressed the slow e.p.s.p. in those neurones in which they did not change the resting membrane potential. The slow e.p.s.p. was increased in amplitude in those neurones hyperpolarized by opioids. Depolarizations resulting from application of barium, substance P or ACh were also enhanced by opioids. Equivalent circuit models in which opioids increase, and substance P or ACh decrease, the same potassium conductance could account for this enhancement. The actions of opioids were prevented or reversed by naloxone (1 nM-1 microM). It is concluded that morphine and enkephalin inhibit the release of ACh and a non-cholinergic transmitter from fibres of the myenteric plexus, and that this may involve a hyperpolarization of presynaptic fibres. Additionally, opioids can interact postsynaptically with other substances which affect membrane potassium conductances.

Acetylcholine↗

PubMedDate not supplied

The effect of substance P on nerve action potential propagation and cholinergic transmission in the myenteric plexus of the guinea-pig ileum.

The effect of substance P on nerve terminals in myenteric plexus of the guinea-pig ileum was investigated. Neurogenic twitches of the myenteric plexus longitudinal muscle strip were recorded. Twitches of the strip portion where excitation involved the most distal parts of cholinergic nerve terminals were more increased by local application of substance P (0.1 and 0.4 nmol/l) than twitches of the portion where excitation involved both distal and proximal parts of nerve terminals. Substance P addition to a portion of the strip conducting nerve action potentials to invade the neighbouring strip portion also augmented twitches of the latter portion so that the interference with the propagation process was considered. The effect of substance P was poorly antagonized by the addition of a substance P antagonist, (D-Arg1, D-Pro2, D-Trp7,9, Leu11)-substance P. Compound nerve action potentials were evoked in strands of fibres of the myenteric plexus by low-frequency train stimulation (1 Hz). The addition of substance P prevented a decrease of the amplitude of responses observed under control conditions. Using high-frequency train stimulation (30 Hz) the amplitude of responses to impulses 2-7 was augmented over that to the first impulse; substance P further increased such facilitation regularly. It seems that substance P might promote nerve action potential invasion of the distal parts of nerve terminals.

Action Potentials↗

PubMed1990

Effect of denervation of the myenteric plexus on gastroduodenal motility in turkeys.

The effect of denervation of portions of the myenteric plexus on initiation and coordination of gastric and duodenal contractions was examined in domestic turkeys. Three areas of the muscular stomach (MS), the isthmus between the glandular stomach (GS) and MS, and the pylorus were denervated by application of 1% benzalkonium chloride. Motor activity of the gastroduodenal organs was monitored for 1 h every other day for 13 days using strain gauge transducers implanted at selected sites. Denervation of the isthmus reduced the frequency of MS and duodenal contractions by 50% and abolished GS contractions. Pyloric denervation did not affect the frequency of GS or MS contractions but abolished duodenal contractions. These results suggest that 1) a driving pacemaker for the gastroduodenal cycle is located in the isthmus, and 2) the myenteric plexus is essential for conduction from the pacemaker to the GS and to the duodenum. Denervation of the medial commissure of the myenteric plexus of the MS significantly impaired the function of the ventral half of the MS. It caused atrophy of the underlying medial thick muscle and significantly decreased contraction amplitude. Denervation at this site also caused an enlargement and impaction of the adjacent caudal thin muscle with food and a significant decrease in contraction amplitude. In contrast, denervation of the lateral commissure enlarged the underlying lateral thick muscle and significantly increased its contraction amplitude. Denervation of the cranial thin muscle delayed contractions of that muscle, causing an asynchronization of thin muscle pair.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2000

Vagus nerve participates in CCK-induced Fos expression in hindbrain but not myenteric plexus.

CCK activates neurons in rat hindbrain and small intestinal myenteric ganglia. Activation of neurons at both sites is mediated through type A CCK receptors. CCK-induced activation of hindbrain neurons is mediated by capsaicin-sensitive vagal fibers. Therefore, it is possible that CCK-induced activation of myenteric neurons also depends upon vagal activation. To test this hypothesis, we examined hindbrain and myenteric neuronal expression of Fos immunoreactivity following CCK injection in rats that had undergone bilateral subdiaphragmatic vagotomy or systemic treatment with capsaicin, a neurotoxin that destroys small unmyelinated primary sensory neurons in the vagus, as well as in other peripheral nerves. We found that CCK (2 or 10 microg/kg) significantly increased Fos expression in both the brains and small intestinal myenteric plexuses of control rats. CCK-induced Fos expression was abolished or attenuated in the brains of vagotomized or capsaicin-treated animals. However, vagotomy or capsaicin treatment did not diminish CCK-induced Fos expression in the small intestinal myenteric plexus. We conclude that CCK-induced activation of intestinal myenteric neurons does not depend on activation of vagal sensory or motor neurons, while activation of neurons in the dorsal hindbrain is mediated, at least in part by CCK-induced activity of small unmyelinated vagal sensory neurons.

Animals↗

PubMed1993

Human recombinant interleukin 1 beta suppresses acetylcholine release from rat myenteric plexus.

BACKGROUND: A marked suppression of acetylcholine (ACh) release from myenteric nerves in the inflamed intestine of rats infected by Trichinella spiralis has been shown. In this model, there is increased expression of interleukin 1 beta (IL-1 beta) in the myenteric plexus. Therefore, the ability of IL-1 beta to alter ACh release in longitudinal muscle-myenteric plexus (LMMP) preparations from noninfected rats was examined. METHODS: LMMP preparations were loaded with [3H]choline before stimulation by KCl or electrical field stimulation. ACh release was recorded by measuring 3H in the superfusate. Experiments were performed in the presence or absence of human recombinant IL-1 beta. RESULTS: IL-1 beta had no immediate effect on the basal or stimulated release of ACh. A marked suppression of ACh release was observed in tissues that had been preincubated with IL-1 beta for 60 minutes or more. The effect of IL-1 beta was concentration and time dependent with maximum suppression occurring with 10 ng/mL of the cytokine after a 90-minute incubation. The action of human recombinant (hr) IL-1 beta was abolished by boiling the cytokine for 20 minutes and was prevented by preincubating the cytokine with neutralizing antibody. The IL-1 beta effect was also blocked by cycloheximide and was spontaneously reversible after 60 minutes. CONCLUSION: It was concluded that IL-1 beta suppresses ACh release via the formation and release of a protein mediator that could be another cytokine, including IL-1. Based on these findings, we consider IL-1 beta a putative mediator of the changes in cholinergic nerve function observed in the inflamed rat intestine.

Acetylcholine↗

PubMed2001

Mucosal acid challenge activates nitrergic neurons in myenteric plexus of rat stomach.

We tested the hypothesis that intrinsic neurons of the rat gastric myenteric plexus can be activated by an acid (HCl) challenge of the mucosa. Activated neurons were visualized by immunohistochemical detection of c-Fos, a marker for neuronal excitation. The neurochemical identity of the neurons activated by the HCl challenge was determined by colocalizing c-Fos with a marker for excitatory pathways, choline acetyltransferase (ChAT), and a marker for inhibitory pathways, nitric oxide synthase (NOS). Two hours after intragastric administration of HCl or saline, stomachs were removed and immunofluorescence triple labeling of myenteric neurons was carried out on whole mount preparations. Treatment with 0.35, 0.5, and 0.7 M HCl induced c-Fos in 8%, 56%, and 64%, respectively, of NOS-positive but not ChAT-positive neurons. c-Fos was also seen in glial cells of HCl-treated rats, whereas in saline-treated animals c-Fos was absent from the myenteric plexus. HCl treatment did not change the proportion of ChAT- and NOS-immunoreactive neurons in the myenteric ganglia. It is concluded that gastric acid challenge concentration-dependently stimulates a subpopulation of nitrergic, but not cholinergic, myenteric plexus neurons, which may play a role in muscle relaxation, vasodilatation, and/or secretion.

Animals↗

PubMed1991

Alkylation with beta-funaltrexamine suggests differences between mu-opioid receptor systems in guinea-pig brain and myenteric-plexus.

1. The effects of pre-incubation with beta-funaltrexamine (beta-FNA) on the binding of [3H]-[D-Ala2, MePhe4, Gly-ol5]enkephalin ([3H]-DAMGO) to homogenates of guinea-pig brain and myenteric-plexus longitudinal muscle have been studied. 2. beta-FNA pretreatment of brain homogenates in Tris-HCl buffer reduced the amount of [3H]-DAMGO binding. This was principally due to a reduction in the maximal number of binding sites measurable. However, approximately 30% of sites labelled by 1 nM [3H]-DAMGO were insensitive to 1 microM beta-FNA. Similar findings were obtained when the alkylation was performed in brain homogenates prepared in Krebs solution buffered with HEPES. 3. beta-FNA pretreatment of whole myenteric-plexus longitudinal muscle strips caused an increase in the IC50 values of mu-agonists, but not of kappa-agonists. However, the binding of [3H]-DAMGO to homogenates of myenteric-plexus longitudinal muscle was not altered by pre-incubation with beta-FNA in Tris-HCl buffer. On the other hand when the pretreatment was carried out in whole tissue in Krebs solution, or in homogenates in the presence of NaCl and Gpp(NH)p, a marked reduction in [3H]-DAMGO binding was observed. 4. These results suggest that a low affinity form of the mu-opioid receptor is the physiologically relevant site for beta-FNA alkylation in the myenteric-plexus and that differences exist between mu-receptor systems in guinea-pig myenteric plexus and brain.

Alkylating Agents↗

PubMed1997

Multiple mechanisms contribute to myenteric plexus ablation induced by benzalkonium chloride in the guinea-pig ileum.

Ablation of rat myenteric plexus with benzalkonium chloride has provided a model of intestinal aganglionosis, but the degenerative responses are not well understood. We examined the effects of this detergent on neurons and glia, including expression of c-Myc, c-Jun, JunB, and c-Fos, and on immunocytes in the guinea-pig ileum. Benzalkonium chloride (0.1%) or saline was applied to the serosal surface of distal ileum. Tissues were analyzed 2, 3, or 7 days later and compared with cyclosporine-treated and untreated animals. More than 90% of myenteric neurons were destroyed in ileal segments 3-7 days after benzalkonium-chloride treatment. Glia withdrew processes from around neurons after 2 days and were mostly gone after 3 days. Neuronal c-Myc began to disappear while c-Fos, c-Jun, and JunB were evident in some neuronal nuclei after 2 or 3 days. After 3 days, widespread apoptosis was evident in the myenteric plexus. Populations of T cells, B cells, and macrophage-like cells in untreated and saline-treated myenteric plexuses were substantially increased 3 and 7 days after benzalkonium-chloride treatment. Cyclosporine delayed significant neuronal loss. We conclude that a variety of degenerative mechanisms may be active in this model, including an immune response which may actively contribute to tissue destruction.

Animals↗

PubMed1995

The neuritogenic effect of myenteric plexus on striatal neurones in co-culture involves nitric oxide.

We reported previously that myenteric plexus explants promoted striatal neurite elongation in co-culture and that this effect was abolished by tetrodotoxin (TTX). Here we demonstrate that the nitric oxide synthase blocker N-nitro-L-arginine methyl ester significantly reduced the neuritogenic effect of the myenteric plexus whereas the nitric oxide donor, sodium nitroprusside (SNP), partially reversed the blocking effect of TTX. 2-Chloroadenosine (2-CA), a stable analogue of adenosine, which is produced following release of ATP from enteric neurones, further enhanced the effect of SNP. Basic fibroblast growth factor or neurotrophin-3 in combination with 2-CA and SNP were only marginally neuritogenic in striatal cultures alone. These results suggest that NO is involved in the trophic effects of myenteric plexus explants on striatal neurones.

2-Chloroadenosine↗