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)

Coated and noncoated vesicles participate in cellular protein transport. Both acetylcholine receptors (AChR) and acetylcholinesterase (AChE) are transported via coated vesicles, some of which accumulate beneath the neuromuscular synapse where AChRs cluster. To investigate the mechanisms by which these proteins are transported during postsynaptic remodeling, we purified coated vesicles from the bovine brain via column chromatography (Sephacryl S-1000) and raised monoclonal antibodies to epitopes of the vesicular membranes enriched in AChE. We assayed for AChE (coated vesicle enriched), hexosaminidase (lysosomal contaminants), NADH cytochrome C reductase (mitochondrial containing), and protein and demonstrated electron microscopically using negative staining that the vesicular fraction contained 95% pure coated vesicles. We then injected coated vesicle fractions and the fractions from which the coat was removed intraperitoneally into mice and obtained three monoclonal antibodies: C-33, C-172, and F-22. On immunoblots of purified vesicles and cultured skeletal muscle, mAb C-33 stained a 180 Kd band and mAb C-172 stained a 100 kd band. MAb F-22 stained 50 kd and 55 kd bands and was not characterized further. Immunofluorescent microscopy with C-33 and C-172 revealed punctate fluorescence whose distribution depends upon the stage of myotube development. Four days after plating, myotubes showed punctate fluorescence throughout the myotube, whereas those stained 8 days after plating showed a punctate perinuclear distribution. Myotubes innervated by ciliary neurons show punctate fluorescence limited to the nuclear periphery and most concentrated around nuclei which line up beneath neuronal processes. This differential vesicular distribution, observed during myotube differentiation and innervation, suggests that these vesicles participate in vesicular membrane traffic.
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PMID:Differential distribution of vesicular carriers during differentiation and synapse formation. 826 42

Arguments are presented in this commentary to show that the model of temperature-nearly-independent binding that we proposed to rationalize the binding characteristics of beta-adrenergic antagonists (Miklavc et al., Biochem Pharmacol 40: 663-669, 1990) in fact provides a consistent interpretation of the temperature-nearly-independent binding constant in all other systems that have been reported in the literature: in the binding of coenzyme NADH to horse liver alcohol dehydrogenase and to octopine dehydrogenase and in the binding of an inhibitor to acetylcholinesterase No such consistent interpretation has been given thus far for any of these systems. It is characteristic of them that the binding takes place in a hydrophobic, sterically constrained environment. One can assume, therefore, that the underlying entropy-driven binding mechanism would reflect the existence and the properties of the steric bottleneck surrounding the binding pocket. We also explain why the temperature effects characteristic of hydrophobic interactions are not found experimentally in these systems, whereas in other, sometimes even structurally similar, systems such temperature effects are clearly present. Further work in necessary to establish more firmly the key features of the temperature-nearly-independent binding mechanism that has been disclosed through our analysis. The binding mechanism in question not only appears in important biochemical systems, but also has the interesting property of being relative unaffected by smaller structural changes.
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PMID:Temperature-nearly-independent binding constant in several biochemical systems. The underlying entropy-driven binding mechanism and its practical significance. 860 66

The cardiac plexus of the Wistar rat was investigated in whole-mount preparations of the atria by NADH-diaphorase staining and by the acetylcholinesterase (AChE) histochemical technique. The plexus lies over the muscular layer of the atria, dorsal to the muscle itself, in the connective tissue of the subepicardium. The plexus contains on average 975 +/- 150 neurons, occurring singly or gathered in packed ganglia. The ganglia are found regularly in certain situations, namely, cranially to the pulmonary veins (44% of total); cranially and to the left of superior vena cava (10%); in the interatrial groove (21%); to the left of the left pulmonary vein (11%); caudally to the pulmonary veins (12%) and in the wall of the coronary sinus (1%). Ganglia are never found on the auricular appendages. For the histochemical demonstration of AChE, the 'direct coloring' copper ferrocyanide method was used. Extrinsic nerves enter the atria along the superior vena cava, along the pulmonary veins and along the coronary sinus, forming ganglion-containing plexuses. From specific sites of these plexuses, nerves proceed to the ganglia located to the left of the superior vena cava, to the ventral and dorsal ventricular wall and to the wall of the right atrium, where they form a delicate plexus accompanying the muscle fibers. Most of the neurons of the plexuses displayed AChE activity in the cytoplasm though they presented different reaction intensities. The distribution of cardiac nerves from groups of neurons located at discrete sites may indicate that postganglionic nerves selectively project to and thus control specific cardiac regions and/or functions.
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PMID:Quantitative study and architecture of nerves and ganglia of the rat heart. 896 Feb 99

The myenteric plexus of the proximal colon, midcolon, and distal colon was studied in mice chronically infected with the Y strain of Trypanosoma cruzi by means of histochemical methods for NADH-diaphorase and acetylcholinesterase (AChE) on whole mount preparations. Ganglia of infected mice displayed an irregular distribution, with neurons severely altered in form and were found side by side with slightly degenerated or morphologically normal ones. Significant reductions of at least 36% in the numbers of neurons were recorded in all regions of the colons of infected animals, especially in the distal colon where the neuron number decreased by more than 44%. Measurements of neuron size suggest that the neuronal destruction caused by T. cruzi affected the medium and large neurons. The small neurons apparently were not affected by the infection. The histochemical demonstration of AChE by the direct coloring copper ferrocyanide method showed that in the control animals, most of the neurons of the plexus displayed AChE activity in the cytoplasm although the neurons showed different reaction intensities. The AChE activity was also present, but at a lower intensity, in the myenteric plexus of the colons of infected animals. These results suggest that the T. cruzi infection affects some categories of neurons and implies that some particular enteric neurotransmitter systems could be affected and the potency of their action upon intestinal function consequently reduced.
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PMID:Morphometry and acetylcholinesterase activity of the myenteric neurons of the mouse colon in the chronic phase of experimental Trypanosoma cruzi infection. 1034 41

To investigate the features of erythrocyte metabolism in extremely immature infants, we assayed 21 enzyme activities and glutathione level in cord erythrocytes from 28 extremely low-birth-weight infants (ELBWI; defined as birth weight <1,000 g). The results were compared with those from normal adults and non-neonatal reticulocyte-rich controls. Statistical analysis revealed that activities of six enzymes (glucosephosphate isomerase, phosphoglycerate kinase, monophosphoglycerate mutase, enolase, glucose-6-phosphate dehydrogenase (G6PD), and glutathione reductase) were significantly higher, and those of eight other enzymes (phosphofructokinase, 6-phosphogluconate dehydrogenase (6PGD), glutathione peroxidase, adenylate kinase, adenosine deaminase, acetylcholinesterase, NADH methemoglobin reductase, and catalase) were lower in ELBWI taking their marked reticulocytosis into consideration. The 6PGD/G6PD ratio, which is consistently unchanged under various physiological and pathological conditions, was markedly reduced in ELBWI. Our results support the previous reports that neonatal erythrocytes have a unique metabolic pattern which is different from that of adult erythrocytes, and also suggest that the 6PGD/G6PD ratio might be an index for the developmental immaturity of fetal erythrocytes. This is the first report describing the pattern of erythrocyte enzyme activities in ELBWI.
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PMID:Erythrocyte enzyme activities in cord blood of extremely low-birth-weight infants. 1050 2

We carried out this study with the purpose of analyzing the density of neurons of the myenteric plexus in the mesenteric, intermediate and antimesenteric regions of the ileum of rats. Whole-mounts stained with four different techniques were employed. Through countings under optic microscope in an area of 8.96 mm2 we found the following neuronal means with the techniques of Giemsa, NADH-diaphorase histochemistry, NADPH-diaphorase and acetylcholinesterase, respectively: mesenteric region 2144.40+/-161.05, 1657.80+/-88.23, 473.80+/-19.62, 905.25+/-22.40; intermediate region 1790.60+/-128.24, 1265.20+/-141.17, 371.30+/-27.84, 770.25+/-33.12; antimesenteric region 1647.0+/-76.67, 981.80+/-68.04, 298.50+/-22.75, 704.50+/-69.38. We conclude that there is a variation of neuronal density around the intestinal circumference and this fact independs on the technique used to stain the neurons, and that in a single region the neuronal density varies with the technique employed. We also call attention for the identification of the site were countings were carried out, so that the results of research in this area are not compromised.
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PMID:Regional differences in the number and type of myenteric neurons of the ileum of rats: a comparison of techniques of the neuronal evidentiation. 1129 32

The effects of dehydroepiandrosterone, estradiol and testosterone on 1-methyl-4-phenylpyridium (MPP+)-induced neurotoxicity of the nigrostriatal dopaminergic system were examined in rat. They were subjected to a unilateral intrastriatal infusion of the following treatment conditions: MPP+ alone or co-injection of MPP+ plus each hormone. Four days after injection, concentrations of dopamine and their metabolites were determined from the corpus striatum. To corroborate the neurochemical data an immunohistochemical analysis of tyrosine hydroxylase-immunoreactive fibers and acetylcholinesterase histochemistry in the striatum was performed. Moreover, we performed a dose-response study of the three hormones on the high-affinity dopamine transport system in rat striatal synaptosomes. Rats co-injected within the striatum with MPP+ and either dehydroepiandrosterone or estradiol had significantly greater concentrations of dopamine and less tyrosine hydroxylase-immunoreactive fibers and acetylcholinesterase fiber density loss compared with their respective controls. In addition, 4 days after injection, the brain was fixed and cut into coronal sections, and was immunostained with major histocompatibility complex class II antigens for activated microglia, and glial fibrillary acidic protein for activated astrocytes. Dehydroepiandrosterone also attenuated microglial cell activation. In contrast, testosterone showed reductions in dopamine concentrations similar to those obtained by MPP+. The protective effect of dehydroepiandrosterone against the MPP+ neurotoxic dopaminergic system may be produced by its partial prevention of MPP+ inhibition of NADH oxidase activity, whereas the estradiol may function as a neuroprotectant by reducing the uptake of MPP+ into dopaminergic neurons. Our findings we suggest indicate that dehydroepiandrosterone and estradiol by a non-genomic effect may have an important modulatory action, capable of attenuating degeneration within the striatum, and in this way serve as neuroprotectants of the nigrostriatal dopaminergic system.
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PMID:Comparative study of the neuroprotective effect of dehydroepiandrosterone and 17beta-estradiol against 1-methyl-4-phenylpyridium toxicity on rat striatum. 1182 67

THE ALDEHYDES INTRODUCED IN THIS PAPER AND THE MORE APPROPRIATE CONCENTRATIONS FOR THEIR GENERAL USE AS FIXATIVES ARE: 4 to 6.5 per cent glutaraldehyde, 4 per cent glyoxal, 12.5 per cent hydroxyadipaldehyde, 10 per cent crotonaldehyde, 5 per cent pyruvic aldehyde, 10 per cent acetaldehyde, and 5 per cent methacrolein. These were prepared as cacodylate- or phosphate-buffered solutions (0.1 to 0.2 M, pH 6.5 to 7.6) that, with the exception of glutaraldehyde, contained sucrose (0.22 to 0.55 M). After fixation of from 0.5 hour to 24 hours, the blocks were stored in cold (4 degrees C) buffer (0.1 M) plus sucrose (0.22 M). This material was used for enzyme histochemistry, for electron microscopy (both with and without a second fixation with 1 or 2 per cent osmium tetroxide) after Epon embedding, and for the combination of the two techniques. After fixation in aldehyde, membranous differentiations of the cell were not apparent and the nuclear structure differed from that commonly observed with osmium tetroxide. A postfixation in osmium tetroxide, even after long periods of storage, developed an image that-notable in the case of glutaraldehyde-was largely indistinguishable from that of tissues fixed under optimal conditions with osmium tetroxide alone. Aliesterase, acetylcholinesterase, alkaline phosphatase, acid phosphatase, 5-nucleotidase, adenosine triphosphatase, and DPNH and TPNH diaphorase activities were demonstrable histochemically after most of the fixatives. Cytochrome oxidase, succinic dehydrogenase, and glucose-6-phosphatase were retained after hydroxyaldipaldehyde and, to a lesser extent, after glyoxal fixation. The final product of the activity of several of the above-mentioned enzymes was localized in relation to the fine structure. For this purpose the double fixation procedure was used, selecting in each case the appropriate aldehyde.
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PMID:Cytochemistry and electron microscopy. The preservation of cellular ultrastructure and enzymatic activity by aldehyde fixation. 1397 66

The etiology of neuronal intestinal dysplasia remains largely unknown. There is, however, supporting evidence of the existence of Hirschprung's disease or chronic intestinal obstruction associated with neuronal intestinal dysplasia. With the aim of investigating the possible development of neuronal intestinal dysplasia linked to chronic intestinal obstruction, we have examined the enteric nervous system response to long-term obstruction in a rat model. Three different surgical techniques were tested in Wistar male rats. In animals that survived longer than the cutoff chronic intestinal obstruction point (6 weeks), full-thickness biopsies and acetylcholinesterase (AChE), NADH, hematoxylin-eosin, and anti-S100 protein stainings were performed. The results of our model indicate that chronic intestinal obstruction induced different degrees of enteric nervous system dysplasia, including histological features of neuronal intestinal dysplasia. The relationship between chronic intestinal obstruction and anomalies of the enteric nervous system, including neuronal intestinal dysplasia, needs to be further studied.
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PMID:Evidence of secondary neuronal intestinal dysplasia in a rat model of chronic intestinal obstruction. 1476 26

We investigated possible changes in bioenergetics at the rostral ventrolateral medulla (RVLM), a medullary site where sympathetic vasomotor tone originates and where the organophosphate poison mevinphos (Mev) acts to elicit cardiovascular intoxication. In Sprague-Dawley rats maintained under propofol anesthesia, microinjection bilaterally of Mev (10 nmol) into the RVLM induced progressive hypotension that was accompanied by an early augmentation (80-100 min post-Mev; Phase I), followed by a decrease (>100 min post-Mev; Phase II) in the power density of the vasomotor components (0-0.8 Hz) in systemic arterial pressure (SAP) signals. Enzyme assay revealed that local application of Mev into the RVLM also significantly and progressively depressed the activity of NADH cytochrome c reductase (marker for Complexes I and III) and cytochrome c oxidase (marker for Complex IV) in the mitochondrial respiratory chain of the RVLM, but not the heart. On the other hand, the activity of succinate cytochrome c reductase (marker for Complexes II and III) remained unaltered. Both the cardiovascular consequences and depression of mitochondrial respiratory chain enzymes elicited by Mev were significantly antagonized on comicroinjection of atropine (3.5 or 7 nmol) bilaterally into the RVLM. We conclude that Mev adversely effects cardiovascular control by acting as a cholinesterase inhibitor in the RVLM, whose neuronal activity is intimately related to the death process. The resulting accumulation of acetylcholine and prolonged activation of muscarinic receptors in the RVLM is manifested by a selective dysfunction of respiratory enzyme Complexes I and IV in the mitochondrial respiratory chain that underlies cardiovascular toxicity associated with organophosphate poisons such as Mev.
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PMID:Depression of mitochondrial respiratory enzyme activity in rostral ventrolateral medulla during acute mevinphos intoxication in the rat. 1517 37


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