Disease relevance of Myenteric Plexus

• RESULTS: In colitis, both topical budesonide and systemic IL-1ra treatments attenuated the suppression of KCl-evoked 3H release from longitudinal muscle myenteric plexus in both inflamed and noninflamed segments [1].
• These results suggest that streptozotocin-induced diabetes mellitus is associated with defective cholinergic neuromuscular transmission in the myenteric plexus of the distal small intestine [2].
• Regional distribution of endogenous gamma-aminobutyric acid (GABA), its synthesizing enzyme, glutamic acid decarboxylase (GAD), and metabolic enzyme, GABA transaminase (GABA-T), were determined in the intestinal tract of guinea pigs and cats and the findings compared with the number of ganglion cells in Auerbach's plexus [3].
• Enterotoxin Escherichia coli STa activates a nitric oxide-dependent myenteric plexus secretory reflex in the rat ileum [4].
• The naloxone-induced contracture appears to be mediated mainly by the release of acetylcholine, and to a minor extent by another spasmogenic substance from the myenteric plexus [5].

High impact information on Myenteric Plexus

• The majority of ganglia in the myenteric plexus possess both HO2 and neuronal NO synthase (NOS) [6].
• Defects in myenteric plexus neurotransmission occur both in mice with targeted deletion of genes for HO2 and neuronal NOS [6].
• Mice that lack a functional Kit receptor fail to develop the network of interstitial cells of Cajal associated with Auerbach's plexus in the mouse small intestine and do not generate slow wave activity [7].
• Evidence that substance P is a neurotransmitter in the myenteric plexus [8].
• Furthermore, we have measured the levels of endogenous GABA in strips of taenia coli containing the myenteric plexus [9].

Chemical compound and disease context of Myenteric Plexus

• Activation of neurons in the inferior mesenteric ganglion (IMG) was assessed using c-fos, JunB, and c-Jun expression in the guinea pig IMG and colonic myenteric plexus during mechanosensory stimulation and acute colitis in normal and capsaicin-treated animals [10].
• G proteins have been implicated in the development of opioid dependence of the guinea pig myenteric plexus as chronic fentanyl elevates G0/i alpha and pertussis toxin prevents this phenomenon [11].
• 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 [12].
• These results indicate that the contraction observed in the unstimulated part may have been caused by acetylcholine release from cholinergic nerves as a result of conduction of the oral part excitation by DMPP along cholinergic nerve fibers; ascorbate may have affected the ganglion cells in Auerbach's plexus to potentiate the action of DMPP [13].
• One of the major tea catechins, (-)-epigallocatechin gallate (EGCG at concentrations from 1 to 20 microM), was applied by superfusion to examine its effect on cholinergic ganglion transmission in the myenteric plexus [14].

Biological context of Myenteric Plexus

• Neurturin-deficient (NTN-/-) mice generated by homologous recombination are viable and fertile but have defects in the enteric nervous system, including reduced myenteric plexus innervation density and reduced gastrointestinal motility [15].
• Both groups of opioids caused presynaptic inhibition of acetylcholine release in the myenteric plexus, depressing the amplitude of the fast excitatory postsynaptic potential [16].
• Interaction of loperamide with [3H]naloxone binding sites in guinea pig brain and myenteric plexus [17].
• In summary, we have identified a population of mechanosensory S-neurons in the myenteric plexus of the distal colon which appear to be largely stretch sensitive, rather than muscle-tension sensitive, since they generate ongoing trains of action potentials in the presence of nifedipine [18].
• It is postulated that beta-pre-protachykinin is processed to substance P, neurokinin A, and neuropeptide K in the cell bodies of myenteric plexus neurons but that conversion of neuropeptide K to neurokinin A takes place during packaging into storage vesicles for axonal transport [19].

Anatomical context of Myenteric Plexus

• These data indicate that cisapride facilitates cholinergic transmission in the myenteric plexus of guinea pig ileum and that this effect may be at least partially responsible for the increased propulsive efficiency observed in ileal segments [20].
• The VIP levels were measured biochemically in tissue consisting of the smooth muscle layers and myenteric plexus [21].
• Substance P fibers arise in part from the overlying submucous plexus and in part from the overlying myenteric plexus [22].
• The present study has demonstrated that the majority of NPYI fibers in the myenteric plexus and along the blood vessels in the muscle layers originate from NPYI cell bodies located in the celiac ganglion, which also contains noradrenaline [23].
• In situ hybridization experiments revealed that BDNF mRNA was made by visceral epithelial cells, several types of smooth muscle, and neurons of the myenteric plexus [24].

Associations of Myenteric Plexus with chemical compounds

• Slow synaptic excitation mediated by serotonin in Auerbach's plexus [25].
• In the isolated myenteric plexus, we have measured the specific activity of glutamic acid decarboxylase (GAD; EC 4.1.1.15), the enzyme responsible for conversion of glutamic acid to GABA in GABAergic neurones, and assessed the ability of this tissue to accumulate 3H-GABA newly synthesised from 3H-glutamic acid [9].
• Cisapride is a prokinetic agent believed to facilitate acetylcholine release from the myenteric plexus of the gut [26].
• These results are consistent with the hypothesis that intestinal inflammation suppresses the release of norepinephrine from the myenteric plexus in the Trichinella-infected rat [27].
• Excitation was enhanced by eserine, and blocked by atropine and tetrodotoxin; this excitation was, therefore, probably mediated by acetylcholine release from cholinergic neurons in the myenteric plexus [28].

Gene context of Myenteric Plexus

• RESULTS: HO-2-like but not HO-1-like immunoreactivity was found in IC networks associated with the myenteric plexus and the deep muscular plexus [29].
• Most of Sstr2-expressing neurons in the myenteric plexus showed nitric oxide synthase (NOS) immunoreactivity [30].
• A weak ET-2-like immunoreactivity was also localized to some neurofibers and the myenteric plexus of the muscle layer, coexpressing with vasoactive intestinal peptide [31].
• The increase in VIP- and GAL-like immunoreactivity, seen in the myenteric plexus of untreated diabetic rat ileum, was not present in the myenteric plexus of ileum from insulin- and aldose reductase inhibitor-treated diabetic rats [32].
• In contrast, the immunosympathectomy had no effect on the pattern of distribution of catecholamine-, calcitonin gene-related peptide (CGRP)- and NPY-containing nerve fibres in the myenteric plexus or on substance P- and CGRP-containing neurones and nerve fibres of the submucous plexus [33].

Analytical, diagnostic and therapeutic context of Myenteric Plexus

• METHODS: To test this hypothesis, we studied nonadrenergic, noncholinergic (NANC) relaxation, NOS activity, NADPH diaphorase histochemistry, NOS immunohistochemistry, NOS immunoblotting, and NOS messenger RNA expression in the gastric myenteric plexus of spontaneously diabetic biobreeding/Worcester (BB/W) rats [34].
• The participation of sensory nerves on the release of NO was precluded on the basis that neonatal denervation of the myenteric plexus sensory nerves did not modify the pattern of NO release induced by anandamide and capsaicin [35].
• Effect of lanthanum on the release of acetylcholine from the myenteric plexus and on its activation by ouabain and electrical stimulation [36].
• Immunohistochemistry was used to evaluate the number of neurons immunoreactive for neuronal nitric oxide synthase (NOS) or vasoactive intestinal polypeptide and the density of substance P immunoreactive fibers in the myenteric plexus [37].
• Neurons in the myenteric plexus of the mouse colon were impaled with microelectrodes containing biocytin, their passive and active electrophysiological properties determined, and their responses to activation of synaptic inputs investigated [38].

References