Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gut of silver eels (Anguilla anguilla L.) was investigated in order to describe both the cholinergic and adrenergic intramural innervations, and the localization of possible accessory neuromediators. Histochemical reactions for the demonstration of nicotinamide adenine dinucleotide phosphate, reduced form-(NADPH-)diaphorase and acetylcholinesterase (AChEase) were performed, as well as the immunohistochemical testing of tyrosine hydroxylase, met-enkephalin, substance P, calcitonin gene-related peptide (CGRP), bombesin, vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), somatostatin, cholecystokinin-octapeptide (CCK-8), serotonin, cholineacetyl transferase. The results evidenced a different pattern in comparison with other vertebrates, namely mammals, and with other fish. Both NADPH-diaphorase and AChEase activities were histochemically detected all along the gut in the myenteric plexus, the inner musculature and the propria-submucosa. Tyrosine hydroxylase immunoreactivity was observed in the intestinal tract only, both in the myenteric plexus and in the inner musculature. Several neuropeptides (metenkephalin, CGRP, bombesin, substance P, VIP, NPY, somatostatin) were, in addition, detected in the intramural innervation; some of them also in epithelial cells of the diffuse endocrine system (met-enkephalin, substance P, NPY, somatostatin). Serotonin was only present in endocrine cells. Tyrosine hydroxylase immunoreactivity was present in localizations similar to those of NADPH-diaphorase-reactivity, and in the same nerve bundles in which substance P- and CGRP-like-immunoreactivities were detectable in the intestinal tract. In addition, NADPH-diaphorase-reactive neurons showed an anatomical relationship with AChEase-reactive nerve terminals, and a similar relationship existed between the latter and substance P-like immunoreactivity.
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PMID:Neurotransmitters and putative neuromodulators in the gut of Anguilla anguilla (L.). Localizations in the enteric nervous and endocrine systems. 1109 1

The peristaltic movement of the gut is a function of the alternating contraction and relaxation of circular and longitudinal muscles. This movement is induced by a tendon-like connective-tissue net (TCTN) in the circular and longitudinal muscles, which are both rooted in a connective-tissue plexus layer (CTPL). In children with a therapy-resistant aperistaltic or hypoperistaltic syndrome who had normally-developed enteric innervation, a lack of the TCTN in the muscularis propria was observed. Over the last 2 years, 241 children with chronic constipation were investigated histopathologically; 46 children surgically treated by partial resection of the gut or diagnostically investigated by whole-mount biopsy. Fifteen children had a hypoperistalsis syndrome and 3 had an aperistalsis syndrome. All specimens were native and cut in a cryostat. Enteric innervation was examined by acetylcholinesterase and dehydrogenase reactions. The TCTN in the muscularis propria was stained with picric acid/sirius red. In the children with an aperistalsis syndrome, a complete lack of the TCTN in circular and longitudinal muscles was observed. A CTPL was not developed. The children with a hypoperistalsis syndrome had no CTPL, but had a partly-developed TCTN in the circular and longitudinal muscles, which gradually faded in the direction of the plexus layer. Independent of a well-developed enteric nervous system, a lack of the TCTN in longitudinal and circular muscles and a missing CTPL (aplastic desmosis) abolishes the coordinated peristaltic movement of the gut. An isolated lack of the CTPL in the myenteric plexus (hypoplastic desmosis) results in a hypoperistalsis syndrome. An anomaly of the TCTN in the muscularis propria disturbs gut-muscle mechanics, and is another cause of gut dysmotility.
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PMID:New pathogenetic aspects of gut dysmotility in aplastic and hypoplastic desmosis of early childhood. 1131 73

Acute colonic pseudo-obstruction (Ogilvie's syndrome) can be defined as a clinical condition with symptoms, signs and radiological appearance of acute large bowel obstruction unrelated to any mechanical cause. Recent reports of the efficacy of cholinesterase inhibitors in relieving acute colonic pseudo-obstruction have fuelled interest in the pharmacological treatment of this condition. The aim of the present review is to outline current perspectives in the pharmacological treatment of patients with acute colonic pseudo-obstruction. The best documented pharmacological treatment of Ogilvie's syndrome is intravenous neostigmine (2-2.5 mg), which leads to quick decompression in a significant proportion of patients after a single infusion. However, the search for new colokinetic agents for the treatment of lower gut motor disorders has made available a number of drugs that may also be therapeutic options for Ogilvie's syndrome. Among these agents, the potential of 5-hydroxytryptamine-4 receptor agonists and motilin receptor agonists is discussed.
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PMID:Review article: the pharmacological treatment of acute colonic pseudo-obstruction. 1168 85

Confocal laser scanning microscopy (CLSM) was used to examine molecules related to the cholinergic neurotransmission system and detected at all the larval stages of Paracentrotus lividus, by histochemical and immunohistochemical methods. CLSM, providing spatial resolution of the cells located both at the larval surface and at depth, allows a complete mapping in a three-dimensional volumetric frame. At early larval stages acetylcholinesterase- as well as choline acetyltransferase-like molecules were found mainly in the gut wall cells, and along the ciliary bands of the arms, together with muscarinic acetylcholine receptors. At perimetamorphic stages, cholinergic molecules were present in the ciliate strands along the arms, in the larval body and in the rudiment. At metamorphosis, positivity to cholinergic molecules translocated to the juvenile, where a high frequency of mAChR- and ChAT-like positive cells was found.
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PMID:Three-dimensional mapping of cholinergic molecules by confocal laser scanning microscopy in sea urchin larvae. 1174 47

The motor nervous system of adult ascidians consists of neurons forming the cerebral ganglion from which axons run out directly to the effectors, i.e., muscular and ciliary cells. In this study, we analyzed the development of the motor fibers, correlating this with organ differentiation during asexual reproduction in Botryllus schlosseri. We used a staining method for acetylcholinesterase, whose reaction product is visible with both light and electron microscopy and which labels entire nerves, including their thin terminals, making them identifiable between tissues. While the cerebral ganglion is forming, the axons elongate and follow stereotypical pathways to reach the smooth muscle cells of the body, the striated muscle of the heart, and the ciliated cells of the branchial stigmata and the gut. A strict temporal relation links the development of the local neural network with its target organ, which is approached by nerves before the effector cells are fully differentiated. This process occurs for oral and cloacal siphons, branchial basket, gut, and heart. Axons grow through the extracellular matrix and arrive at their targets from different directions. In some cases, the blood sinuses constitute the favorite roads for growing axons, which seem to be guided by a mechanism involving contact guidance or stereotropism. The pattern of innervation undergoes dynamic rearrangements and a marked process of elimination of axons, when the last stages of blastogenesis occur. The final pattern of motor innervation seems to be regulated by axon withdrawal, rather than apoptosis of motor neurons.
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PMID:Development of the motor nervous system in ascidians. 1179 51

Since melatonin receptors are present in the intestines, the possibility that this hormone may affect intestinal motility has been studied in the rat. Sprague-Dawley male rats were given a carmine cochineal powder meal and were injected intraperitoneally with 1, 10, 100, or 1000 microg/kg melatonin. Sixty minutes after treatment, intestinal transit was found to be faster in animals treated with small doses of melatonin (1 or 10 microg/kg) than in saline-injected controls. This effect, however, appear to be clearly reversed with 100 or 1000 microg/kg melatonin. In fact, these doses of the hormone reduced intestinal transit in rats. The nonselective melatonin receptor antagonist, luzindole (administered intraperitoneally in a dose of 0.25 mg/kg, 15 min prior to melatonin injection) totally prevented the accelerating effect of melatonin (10 microg/kg) on intestinal transit. Luzindole per se failed to affect gut motility. Injection of the reversible acetylcholinesterase inhibitor and cholinergic agent, neostigmine, accelerated intestinal transit but failed to influence melatonin effect on this parameter. In contrast, intraperitoneal injection of the muscarinic receptor antagonist atropine delayed intestinal transit per se but did not reduce the stimulating effect of melatonin on this parameter. Intestinal myoelectrical recording revealed that intestinal myoelectrical activity was increased by intraperitoneal injection of melatonin (10 microg/kg). Administration of luzindole totally prevented melatonin-induced increase of intestinal myoelectrical activity. These results indicate that melatonin may affect intestinal motility in rats when administered in small doses. This effect might be mediated by melatonin receptors in the intestines, although the involvement of central receptors for the hormone is also possible.
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PMID:Small doses of melatonin increase intestinal motility in rats. 1235 39

The action of chromatographically pure crystalline muscarine chloride, prepared from Amanita muscaria, has been compared with acetylcholine chloride (ACh) on a number of different organs from a variety of species. Muscarine caused spasm in vivo and in vitro of muscles of the gut, uterus, urinary bladder, and bronchus. It also caused contraction of the horse ureter and carotid artery chain in vitro and slowed the isolated auricles of the guinea-pig and rabbit, and the frog heart.Muscarine caused a drop in blood pressure, although in vitro it produced either constriction or dilatation of the blood vessels of the rabbit ear.All these actions resembled those of acetylcholine, though muscarine was usually more potent. Muscarine effects were readily prevented by atropine sulphate. It had a slight action on the frog rectus abdominis muscle, causing a contracture at high concentrations. Muscarine was destroyed neither by pepsin nor by boiling at any pH. It was inactive by mouth in a monkey in a quantity many times that which would cause poisoning by ingestion of Amanita muscaria in the human being. Muscarine neither inhibited nor was hydrolysed by either true- or pseudo-cholinesterase. Muscarine chloride did not cause paralysis of the neuromuscular junctions of the rat diaphragm or of the cat gastrocnemius.
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PMID:Pharmacological actions of pure muscarine chloride. 1341 51

The dose-limiting toxicity of the highly effective anticancer agent 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxy-camptothecin (irinotecan; CPT-11) is delayed diarrhea. This is thought to be caused by either bacteria-mediated hydrolysis of the glucuronide conjugate of the active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38) or direct conversion of CPT-11 to SN-38 by carboxylesterases (CE) in the small intestine. After drug administration, a very high level of CPT-11 is present in the bile; this is deposited into the duodenum, the region of the gut with the highest levels of CE activity. Hence, it is likely that direct conversion of the drug to SN-38 is partially responsible for the diarrhea associated with this agent. In an attempt to ameliorate this toxicity, we have applied Target-Related Affinity Profiling to identify novel CE inhibitors that are selective inhibitors of the human intestinal enzyme (hiCE). Seven inhibitors, all sulfonamide derivatives, demonstrated greater than 200-fold selectivity for hiCE compared with the human liver CE hCE1, and none was an inhibitor of human acetylcholinesterase or butyrylcholinesterase. Quantitative structure-activity relationship (QSAR) analysis demonstrated excellent correlations with the predicted versus experimental Ki values (r2 = 0.944) for hiCE. Additionally, design and synthesis of a tetrafluorine-substituted sulfonamide analog, which QSAR indicated would demonstrate improved inhibition of hiCE, validated the computer predictive analyses. These and other phenyl-substituted sulfonamides compounds are regarded as lead compounds for the development of effective, selective CE inhibitors for clinical applications.
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PMID:Discovery of novel selective inhibitors of human intestinal carboxylesterase for the amelioration of irinotecan-induced diarrhea: synthesis, quantitative structure-activity relationship analysis, and biological activity. 1515 27

The embryotoxic potential of chlorpyrifos (CPF) and malathion (MTN), two organophosphorus insecticides (OPs), was evaluated by modified Frog Embryo Teratogenesis Assay-Xenopus (FETAX). CPF and MTN were not embryolethal even at the highest concentration tested (6000 microg/l), but both exhibited a powerful teratogenicity. The probit analysis of malformed larva percentages showed a TC(50) of 161.54mug/l for CPF, and a TC(50) of 2394.01 microg/l for MTN. Therefore, CPF teratogenicity was about 15 times higher than MTN. Larvae of both exposed groups were mainly affected by ventral and/or lateral tail flexure coupled with abnormal gut coiling. Histopathological diagnosis displayed abnormal myotomes and myocytes with marked hypertrophies localized at the cell extremity, probably due to a break away of myofibril extremities at the intersomitic junction level. We speculate that this muscular damage was related to inhibition of acetylcholinesterase that showed a clear concentration-response in CPF and MTN exposed larvae. The teratogenic effects of these anti-cholinesterase compounds on Xenopus laevis myogenesis suggest a possible role played by OPs on induction of congenital muscular dystrophy.
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PMID:Comparative teratogenicity of chlorpyrifos and malathion on Xenopus laevis development. 1555 Feb 76

The aim of this investigation was to see if the crude extract of Sarcococca saligna (Ss.Cr) contains chemicals with gut function inhibitory activity by using in vitro and in vivo assays. Ss.Cr caused a dose-dependent (0.03 - 3 mg/mL) inhibitory effect on K+-induced contractions in rat stomach fundus, guinea-pig ileum and rabbit jejunum preparations. The calcium channel blocking(CCB) activity was confirmed when Ss.Cr caused a rightward shift in the Ca++ dose-response curves. It also potentiated, at lower do-ses (0.001 - 0.03 mg/mL), the contractile effect of a fixed dose of acetylcholine (ACh), similar to physostigmine, and suppressed the effect of ACh at higher doses (0.3 - 1.0 mg/mL). Both Ss.Cr and physostigmine inhibited acetylcholinesterase (AChE), in the in vitro assay, confirming the AChE inhibitory activity. In the in vivo studies, Ss.Cr exhibited antidiarrheal and antisecretory activities against castor oil-induced diarrhea and intestinal fluid accumulation in mice. Characteristic steroidal compounds of the plant (saracocine, saracodine, saracorine and alkaloid-C), exhibited a similar combination of AChE inhibitory and CCB activities. Thus this study provides a sound mechanistic base for some of the traditional uses of the plant in hyperactive gut states, in addition to providing the first evidence for verapamil to possess additional AChE inhibitory activity. Furthermore, these characteristic compounds with dual activity may be good candidates for further studies on their usefulness in Alzheimer's disease.
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PMID:Presence of antispasmodic, antidiarrheal, antisecretory, calcium antagonist and acetylcholinesterase inhibitory steroidal alkaloids in Sarcococca saligna. 1578 98


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