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PubMed1982

Identification of and interactions between noradrenergic and serotonergic neurites in the myenteric plexus.

Interactions between enteric noradrenergic and serotonergic neurites in the myenteric plexus were examined. The influence of exogenous norepinephrine (NE) and endogenously released NE on the release of 3H-serotonin (3H-5-HT) from electrically stimulated, everted segments of guinea pig small intestine were analyzed. In addition, methods were employed to permit the ultrastructural identification of enteric serotonergic and noradrenergic neurites. These included electron microscopic radioautographic localization of 3H-5-HT in gut from animals treated with 6-hydroxydopamine (6-HD; 100 mg/kg) and examination of NaMnO4-fixed tissue from animals given desmethylimipramine and the indolic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT). Exogenous NE antagonized the stimulated release of 3H-5-HT; this action was mediated through alpha adrenoceptors. Evidence was obtained, however, that endogenous NE liberated from sympathetic postganglionic nerve terminals had a different action on the stimulated release of 3H-5-HT from that of exogenous NE. Endogenous NE appeared to facilitate 3H-5-HT release through an action on beta adrenoceptors. Terminals identified as probably serotonergic by radioautographic labeling with 3H-5-HT or by loading with 5,7-DHT were most often found to end on neuronal somata or proximal dendrites. Synaptic specializations were found by radioautography in these locations. Terminals, dendrites, and cell bodies that took up 5,7-DHT could be identified in NaMnO4-fixed material that also permitted the simultaneous recognition of noradrenergic varicosities. Apparent noradrenergic-serotonergic axoaxonic contacts were found by means of this double-labeling technique. Together with the results of the experiments on the release of 3H-5-HT, these anatomical observations suggest that noradrenergic axons form facilitatory axoaxonic synapses with enteric serotonergic neurons.

5,7-Dihydroxytryptamine↗
PubMed1982

Muscarinic synaptic potentials in guinea-pig myenteric plexus neurones.

1. Intracellular recordings were made from neurones in the myenteric plexus of the guinea-pig ileum in vitro. 2. A single pulse stimulus to the presynaptic fibres entering a myenteric ganglion elicited a fast excitatory post-synaptic potential (e.p.s.p.) in type 1 (S) cells: in about one-quarter of cells this was followed by a slow e.p.s.p. 3. The slow e.p.s.p. had a latency of 122 ms and a total duration of 3-15 s. It was reversibly abolished by hyoscine (1 microM). 4. Both the fast e.p.s.p. and the slow e.p.s.p. could be mimicked by ionophoretic application of a single brief pulse of acetylcholine (ACh) to the neurone soma. The depolarization which mimicked the fast e.p.s.p. was reversibly blocked by hexamethonium. The depolarization which mimicked the slow e.p.s.p. was reversibly blocked by hyoscine. 5. Type 2 (AH) neurones did not show fast or slow e.p.s.p.s in response to a single pulse stimulus. Stimuli comprising many pulses (typically 10 Hz for 3 s) evoked a slow e.p.s.p. in which the initial portion was partly blocked by hyoscine, but which was predominantly non-cholinergic.

Acetylcholine↗
PubMed1988

Projections of submucosal neurons to the myenteric plexus of the guinea pig intestine: in vitro tracing of microcircuits by retrograde and anterograde transport.

The enteric nervous system (ENS) can mediate reflex activity without input from the brain or spinal cord. The ENS thus contains intrinsic primary afferent neurons that link mucosal sensory receptors with motor neurons in the myenteric plexus. The intrinsic primary afferent neurons of the gut have not yet been identified. Although the submucosal plexus is known to innervate the mucosa, where enteric sensory receptors are located, no submucosal to myenteric projections have previously been found. In order to determine whether such projections exist, the submucosal plexus was examined following the microinjection of a retrograde tracer (Fluoro-Gold or 4-acetoamido, 4'-isothiocyanostilbene-2,2'-disulphonic acid [SITS]) into single myenteric ganglia. In addition, the myenteric plexus was studied following the iontophoretic injection of an anterograde tracer (Phaseolus vulgaris leucoagglutinin; [PHA-L]) into single submucosal ganglia. Ganglia were visualized by use of differential interference contrast optics and were injected from the beveled tip of a glass micropipette; 2.5-3.0 hours were allotted for retrograde and 20-24 hours (under culture conditions) for anterograde transport. In the myenteric plexus, a small number of the neurons of each injected ganglion were fluorescent and additional neurons in distant myenteric ganglia (predominantly orad) were also retrogradely labeled. About five to six submucosal neurons deep to but not directly underneath the injected myenteric ganglion were labeled by Fluoro-Gold or SITS and only rarely was there more than one labeled neuron in a submucosal ganglion. When control injections of Fluoro-Gold were placed into the muscle instead of a ganglion, some myenteric neurons near the injection site became labeled indicating an innervation of the circular muscle by myenteric neurons; however, there was no labeling of neurons in the submucosal plexus. Similarly, if connections between the myenteric and submucosal plexuses were severed before injecting Fluoro-Gold, no submucosal neurons were labeled. Following injection of PHA-L into a single submucosal ganglion, small-diameter axons were labeled in approximately 2 myenteric ganglia as well as in several distant submucosal ganglia (mainly anal and circumferential to the injection site). Additional labeled fibers traveled with blood vessels or surrounded mucosal crypts. It is concluded that submucosal neurons project to the myenteric plexus as well as to the mucosa and to one another. These observations are consistent with the hypothesis that at least some intrinsic enteric primary afferent neurons reside in the submucosal plexus.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1982

Depolarization-induced release of adenosine 5'-triphosphate from isolated varicosities derived from the myenteric plexus of the guinea pig small intestine.

In order to study the release of ATP from a neuronal preparation thought to be "purinergic," isolated varicosities were prepared from myenteric plexus by mincing and homogenizing the longitudinal muscle of guinea pig ileum in 0.32 M sucrose. The presence of varicosities within the crude preparation (P2), isolated by differential centrifugation, was confirmed by electron microscopy and by the presence of occluded lactate dehydrogenase as a cytoplasmic marker. Varicosities were purified further from the P2 fraction on a discontinuous sucrose density gradient and characterized morphologically. Varicosities resembling cholinergic, "purinergic," and adrenergic axonal terminals were identified. The release of ATP from both crude and purified varicosities was detected by monitoring the light produced when the released ATP reacted with firefly luciferin-luciferase which was present in the incubation medium. Elevated extracellular K+ or Rb+ caused the release of ATP, whereas elevated Na+ and Li+ did not. The release of ATP by either K+ or by the depolarizing drug, veratridine, was Ca2+ dependent. This requirement of extracellular Ca2+ for veratridine-induced release of ATP from isolated myenteric varicosities contrasted strikingly with that for brain synaptosomes, where the release of ATP induced by veratridine was increased rather than decreased in a Ca2+-free medium. The characteristics of ATP release from myenteric varicosities are consistent with a possible neurotransmitter function for ATP in myenteric plexus, although it is also possible that ATP is co-released with some other neurotransmitter.

Adenosine Triphosphate↗
PubMed1989

Light and electron microscopic localization of GABA-like immunoreactivity in myenteric plexus of chicken.

Whole-mounts of 1-day-old chicken midgut were incubated with an antiserum against GABA-glutaraldehyde-BSA conjugate. The immunoreaction was visualized by using the peroxidase-antiperoxidase method, and processed for consecutive light and electronmicroscopic observation. GABA was selectively localized in some of the varicose and nonvaricose nerve fibres of the myenteric plexus. The varicose fibres formed dense networks within the myenteric ganglia, some of which--mainly in duodenum--also contained immunopositive nerve cell bodies. Some of the varicose fibres projected out from the myenteric plexus into the circular muscle layer. At the electronmicroscopic level, labelled axon terminals formed synaptic contact with unlabelled perikarya and vica versa. At the same time, no labelled terminals were found on immunostained cells. In a few cases, axon terminals with GABA positivity were situated close to the smooth muscle cells in the circular muscle layer, suggesting a prejunctional GABA effect on the neighbouring nerve terminals on the release of their transmitters.

Animals↗
PubMed2003

Actions of orexin-A in the myenteric plexus of the guinea-pig small intestine.

Orexins and orexin-receptors are localized by displaying their immunoreactivity in the enteric nervous system. Intracellular recordings were made from isolated myenteric neurons to investigate actions of orexin-A in the myenteric plexus of the guinea-pig ileum. Superfusion of orexin-A caused membrane depolarizations in a subset of S and AH neurons. Orexin-A responses were preserved in Ca2+ free/high Mg2+ solution and associated with an increase in input membrane resistance; their reversal potential was about -90 mV. Orexin-A augmented nicotinic fast EPSPs, whereas it did not affect the postsynaptic sensitivity to acetylcholine; this indicates that orexin-A increased the presynaptic release of acetylcholine. In conclusion, orexin-A contributes in the regulation of gut motility via its pre- and postsynaptic actions in the myenteric plexus.

Animals↗
PubMedDate not supplied

The myenteric plexus of the rat colon: a methodological approach for scanning electron microscopical study.

In the present research four different procedures were tested for the Scanning Electron Microscopic identification of Auerbach's myenteric plexus in the distal colon of the rat. The specimens were processed as follows: enzymatic and chemical digestion (trypsin and HCl); fixation with glutaraldehyde; fixation and staining with zinc iodide/osmium tetroxide (ZIO); fixation and staining with zinc iodide/osmium tetroxide (ZIO) followed by maceration in NaOH solution. All the procedures required microdissection to separate the different layers of the colonic wall. Light microscopic controls were prepared with the ZIO technique. Among the methods utilized, fixation and staining with ZIO appeared to be by far the best as regards the preservation of the architectural arrangement of the myenteric plexus as well as of the fine structural details.

Animals↗
PubMed1987

Distribution of myelinated nerves in ascending nerves and myenteric plexus of cat colon.

The parts of the colon differ in motor function and in responses to extrinsic and intrinsic nerve stimulation. The distribution of myelinated nerve fibers in the colonic myenteric plexus is not known. Because these fibers might be largely extrinsic in origin, their distribution might indicate the domain of influence of extrinsic nerves and help to explain the different behaviors of the different parts of the colon. Myelinated fibers were examined by electron microscopy in cross sections of the ascending nerves and in myelin-stained whole-mount preparations in the colon. The ascending nerves are much like one another. They have the structure of peripheral nerves, not that of myenteric plexus. The proportion of myelinated fibers in the ascending nerves declines rostrad with no uniform change in total nerve fiber number. Cross-sectional areas of ascending nerves, 3,304 to 7,448 microns 2; total number of nerve fibers per profile, 703-2,651; and mean myelin coat thickness, 0.45 +/- 0.01 micron, do not change uniformly along the ascending nerves. Myelinated fibers are about 2% of total fibers in the extramural colonic nerves, 7-9% in the ascending nerves in the sigmoid colon, and 2-3% at the rostrad ends of the ascending nerves in the transverse colon. Blood vessels lie at the core of each ascending nerve and on the nerve sheath. Myelinated fibers in the ascending nerves degenerate after section of colonic branches of the pelvic plexus and after section of the pudendal nerves, indicating that myelinated nerves reach the colon through both pathways.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1991

Immunohistochemical identification of cholinergic neurons in the myenteric plexus of guinea-pig small intestine.

It is well established that acetylcholine is a neurotransmitter at several distinct sites in the mammalian enteric nervous system. However, identification of the cholinergic neurons has not been possible due to an inability to selectively label enteric cholinergic neurons. In the present study an immunohistochemical method has been developed to localize choline acetyltransferase, the synthetic enzyme for acetylcholine, in order that cholinergic neurons can be visualized. The morphology, neurochemical coding and projections of cholinergic neurons in the guinea-pig small intestine were determined using double-labelling immunohistochemistry. These experiments have revealed that many myenteric neurons are cholinergic and that they can be distinguished by their specific combinations of immunoreactivity for neurochemicals such as calretinin, neurofilament protein triplet, substance P, enkephalin, somatostatin, 5-hydroxytryptamine, vasoactive intestinal peptide and calbindin. On the basis of their previously described projections, functional roles could be attributed to each of these populations. The identified cholinergic neurons are: motorneurons to the longitudinal muscle (choline acetyltransferase/calretinin); motorneurons to the circular muscle (choline acetyltransferase/neurofilament triplet protein/substance P, choline acetyltransferase/substance P and choline acetyltransferase alone); orally directed interneurons in the myenteric plexus (choline acetyltransferase/calretinin/enkephalin); anally directed interneurons in the myenteric plexus (choline acetyltransferase/somatostatin, choline acetyltransferase/5-hydroxytryptamine, choline acetyltransferase/vasoactive intestinal peptide); secretomotor neurons to the mucosa (choline acetyltransferase/somatostatin); and sensory neurons mediating myenteric reflexes (choline acetyltransferase/calbindin). This information provides a unique opportunity to identify functionally distinct populations of cholinergic neurons and will be of value in the interpretation of physiological and pharmacological studies of enteric neuronal circuitry.

Animals↗
PubMedDate not supplied

Phosphatase activity in the myenteric plexus.

Intense and very intense reactions were obtained for acid phosphatase, calcium activated ATP-ase (pH 9.4), magnesium activated ATP-ase (pH 7.2) and glucose-6-phosphatase in the cytoplasms of the myenteric plexus nerve cells of the small intestine of Macacus rhesus and rabbit. Nucleotidase activity was moderate or slight and unspecific alkaline phosphatase activity absent. Both ATP-ases presented an intense activity in the myenteric plexus nerve cells of human fetuses 30, 33, and 34 weeks old; 5-nucleotidase activity, slight in the 30-week-old fetuses became more intense in the 33- and 34-week-old fetuses. The satellite neuroglial cells, nerve fibers and blood capillaries presented negative alkaline phosphatase reactions and intense or very intense activities of the other phosphatases.

5'-Nucleotidase↗
PubMed1989

Effects of Pertussis Toxin Suggest a Role for G-Proteins in the Inhibition of Acetylcholine Release from Rat Myenteric Plexus by Opioid and Presynaptic Muscarinic Receptors.

(1) Longitudinal muscle preparations of the rat ileum with the attached myenteric plexuses (LMMPs) were preloaded with (3H)choline and the effects of drugs on the depolarization-evoked release of radioactivity corresponding to (3H) acetylcholine ((3H)ACh) were measured. The release of (3H)ACh was inhibited by morphine and the effect of morphine was blocked by naloxone. Morphine had no effect on the release of (3H)ACh in LMMPs from rats that had been injected with pertussis toxin (PTX) 7 days before experiments. (2) Carbamoylcholine applied in the presence of tetrodotoxin inhibited the release of (3H)ACh evoked by depolarization of LMMPs. The effect of carbamoylcholine was absent in LMMPs from rats pretreated with PTX. (3) The effects of PTX indicate that one or more PTX-sensitive G proteins are involved in the chain of events mediating the action of opioid and muscarinic receptors on the release of ACh from the myenteric plexus. It is suggested that the inhibition of ACh release depends on G-protein-mediated coupling of opiod receptors with K+ channels and of muscarinic receptors with Ca2+ channels, but alternative explanations cannot be excluded.

Journal Article↗
PubMed1999

Autoaggressive inflammation of the myenteric plexus resulting in intestinal pseudoobstruction.

After a 3-year history of severe constipation, a 16-year-old girl required surgery to be relieved of impacted stools. Histologic examination showed ganglionitis in the myenteric plexus of the large bowel and ileum, whereas the submucosal plexus was spared. At this time, antineuronal nuclear antibodies (ANNA-1, anti-Hu) were found at high titer in the serum of the patient. One and a half years earlier, a paravertebral ganglioneuroblastoma had been removed. Histologic examination had shown undifferentiated neuroblasts and morphologically mature ganglion cells with both cell types embedded in an inflammatory infiltrate morphologically similar to the lymphoplasmocytic infiltration seen in the myenteric plexus. The patient's serum was found to bind to nuclei of mouse intestinal tract neurons, thus fulfilling defining criteria for ANNA-1. The serum also reacted with antigens of defined molecular weight in a Western blot, thus fulfilling defining criteria for anti-Hu. Expression of the Huantigen could be visualized in the nuclei of the patient's tumor cells by immunohistochemistry. These tests showed that an antitumor inflammatory response was the cause of the bowel disease. This is the first report of a tumor from the neuroblastoma group that caused paraneoplastic intestinal pseudoobstruction. Ganglionitis and subsequent aganglionosis are the hallmark of the morphologic diagnosis which cannot be obtained by suction biopsy in patients with intact submucosal plexus. Instead, serum testing for autoantibodies can reveal the etiology.

Adolescent↗
PubMed1982

[Segmental dilatation of the ileum in a neonate. Study of the myenteric plexus with a silver staining preparation (author's transl)].

A case of segmental dilatation of the ileum in a neonate is reported. Conventional staining methods failed to show any abnormality, but a study of the myenteric plexus with a silver preparation demonstrated reduction in the number of agyrophil neurons and irregular and altered neuron cell bodies. Occurring in a neonate, therefore without previous clinical history, this case, together with various published data suggests that in some cases segmental dilatation of the ileum is due to congenital damage to the myenteric plexus.

Dilatation, Pathologic↗
PubMed1985

Quinacrine-induced dilation of the rat cecum and degeneration of large granular vesicle-containing neurons in the myenteric plexus.

Intraperitoneal injection of quinacrine (100 mg/kg) into rats causes marked dilation of the cecum about one week after the injection, but the jejunum remains its normal size. The morphological changes induced in the myenteric plexus and the longitudinal and circular muscle layers of both the cecum and the jejunum have been examined by fluorescence and electron microscopy 1.5 h to 2 weeks after the injection. In the cecum, 1.5 h after the injection, the granular fluorescence of quinacrine was apparent in many ganglion cells of the myenteric plexus and in the nerve fibers in the muscle layers. In connection with the granular fluorescence, numerous lysosomal dense bodies appeared in ganglion cells and axons, and subsequently the degeneration of the neurons was observed at ultrastructural level. The lysosomal dense bodies often contained many large granular vesicles of 95-140 nm in diameter. The number of lysosomal dense bodies in the axons was greatest 3-7 days after the injection. Although the axon type sensitive to quinacrine could not be specified, axons containing many large granular vesicles were the predominate type. Fibrosis in the outer longitudinal muscle layer was another characteristic resulting from quinacrine administration. Proliferation of the rough-surfaced endoplasmic reticulum and of the Golgi complex and a concomitant decrease in the number of myofilaments became evident in many smooth muscle cells 3-7 days after the injection; the intercellular spaces became enlarged 7 days after quinacrine administration. These changes and the dilation of the cecum showed considerable recovery 2 weeks after the injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Ablation of the myenteric plexus impairs alpha but not beta adrenergic receptor-mediated mechanical responses of rat jejunal longitudinal muscle.

The mechanical responses produced by alpha and beta adrenergic receptor agonists were evaluated in control and myenteric neuron-ablated rat jejunal longitudinal muscle. The myenteric plexus of the jejunum was destroyed by serosal application of benzalkonium chloride (BAC). The beta adrenergic receptor agonists isoproterenol and sulfonterol produced a concentration-dependent relaxation of both control and BAC-treated jejunum. Dose-response curves obtained in control and BAC-treated jejunum were nearly superimposable regardless of the beta agonist used. Isoproterenol-induced relaxation was antagonized by the beta receptor antagonists propranolol and practolol but not by butoxamine. The alpha-1 selective agonists phenylephrine and methoxamine were more potent and efficacious in producing relaxation of control than BAC-treated jejunum. The relaxant responses of methoxamine and phenylephrine in control jejunum were blocked by prazosin but not by yohimbine. The supposed alpha-2 selective agonist clonidine also produced a concentration-dependent, prazosin-sensitive, yohimbine-resistant relaxation which was markedly greater in control than BAC-treated jejunum, consistent with alpha-1 receptor stimulation. Clonidine tested in the presence of prazosin and the alpha-2 selective receptor agonists UK-14,304, M-7 and B-HT 920 all produced a concentration-dependent contraction of control but not BAC-treated jejunum. The contractile response produced by UK-14,304 was antagonized by yohimbine but not by atropine. Our results suggest that in rat jejunal longitudinal muscle: beta adrenergic receptors mediate relaxation and are located on the smooth muscle; alpha-1 adrenergic receptors mediate relaxation and are located on both the smooth muscle and myenteric plexus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1981

Comparative studies of quinacrine-positive neurones in the myenteric plexus of stomach and intestine of guinea-pig, rabbit and rat.

The number of quinacrine-fluorescent nerve cell bodies and the percentage of the ganglion area occupied by this fluorescence within stretch preparations of the myenteric plexus of the stomach and ileum of the guinea-pig, rabbit and rat were assessed. The number of quinacrine-positive cell bodies per cm2 of plexus varied between 1045 in the rabbit ileum to 2633 in the rat stomach, whilst the percentage of the ganglionic area occupied by fluorescence was approximately 10%. The distribution of quinacrine-fluorescent nerve fibres and cell bodies in the myenteric plexus was compared to the distribution of nerves revealed by catecholamine fluorescence and by staining for acetylcholinesterase in the stomach and ileum of all three species. Quinacrine fluorescence appears to be selective for non-adrenergic, non-cholinergic nerves; the possibility that it binds to high levels of ATP is discussed.

Acetylcholinesterase↗
PubMed1997

Nitric oxide synthase (NOS) expression in the myenteric plexus of streptozotocin-diabetic rats.

Nitric oxide (NO) is an important inhibitory neurotransmitter in the gut. Alterations in NO mediated responses have been described in diabetic animals. The presence of nitric oxide synthase (NOS) reflects the potential for NO synthesis and is found in neurons in the myenteric plexus. The aim of this study was to determine changes in nitric oxide synthase (NOS) expression in the myenteric plexus of the gastrointestinal tract of diabetic rats at three months of streptozotocin-induced diabetes, compared to age matched controls, using immunohistochemistry. Diabetic animals showed a decrease in NOS expression in the antrum, with 59.1 +/- 7.3% of neurons being positive for NOS in diabetes compared to 81.2 +/- 4.7% in controls (P < 0.05). NOS expression in duodenum, ileum, and colon of diabetic animals was not statistically different from controls. Decreased expression of NOS in antrum may contribute to altered gastric emptying observed in diabetics.

Animals↗