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

---

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

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.
...
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.
...
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.
...
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.
...
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.
...
PMID:Comparative study of the neuroprotective effect of dehydroepiandrosterone and 17beta-estradiol against 1-methyl-4-phenylpyridium toxicity on rat striatum. 1182 67

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.
...
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.
...
PMID:Depression of mitochondrial respiratory enzyme activity in rostral ventrolateral medulla during acute mevinphos intoxication in the rat. 1517 37

To characterize the extent to which reinnervation potential depends on the duration of denervation, intramuscular neurotization of the gracilis muscle was performed either immediately or 2, 4, 6, and 8 weeks after transection of the obturator nerve. For neurotization, the sciatic nerve was split into three fascicle groups and fixed intramuscularly. Muscle morphology after 6 weeks of regeneration was identified with anti-myosin immunohistochemistry and NADH staining. Newly formed motor endplates were characterized using acetylcholinesterase staining and electron microscopy. Wet muscle weight ratio indicated the functional state of synapses. Depending on the denervation period, three levels of regenerative outcome were evident. Best results were seen after immediate neurotization or after 2 weeks of denervation. Regeneration, although at a significantly lower level, also occurred after denervation periods of 4 and 6 weeks. Regeneration following neurotization after 8 weeks of denervation was negligible. Quantity and quality of motor endplate formation depended on the denervation period. Thus, in special clinical situations intramuscular neurotization within a distinct time window provides a good reconstructive option.
...
PMID:Successful intramuscular neurotization is dependent on the denervation period. A histomorphological study of the gracilis muscle in rats. 1573 1

We investigated weight gain, the size of the small intestine and numbers and sizes of enteric neurons in rats whose mothers had been deprived of protein during pregnancy and who themselves were deprived postpartum. Postnatally, protein deprivation was for 42 days, or for 21 days with refeeding for a further 21 days. Control animals received normal nourishment. Neurons were located by nicotinamide adenine dinucleotide (NADH) diaphorase staining, by acetylcholinesterase (AChE) activity and immunoreactivity for choline acetyltransferase (ChAT). The collagen and elastic fibers in the myenteric ganglia were evaluated histologically. The myenteric ganglia were regular and uniform in the nourished and refed groups. In the undernourished group, the myenteric ganglia were irregularly arranged and the cytoplasm of most of the neurons showed less intense staining for NADH diaphorase, AChE and ChAT. AChE activity and ChAT immunoreactivity showed that most ganglionic neurons were stained in nourished and refed groups, but the neurons of undernourished rats were unstained or moderately stained. The distribution of the connective tissue of the ganglionic capsule was similar in the three groups. There was a decrease in weight of undernourished rats, which was restored in refed rats. The size of the small intestine of the undernourished group was smaller than in the normally fed group, by about 45%, but it was similar in nourished and refed rats. After 42 days of protein deprivation the numbers of neurons that were revealed by NADH diaphorase were fewer than in well nourished rats, but numbers were not different between nourished and refed rats. These observations indicate that protein deprivation alters histological features and acetylcholinesterase activity of neurons and also reduces body weight but these were restored by refeeding.
...
PMID:Effects of pre- and postnatal protein deprivation and postnatal refeeding on myenteric neurons of the rat small intestine: a quantitative morphological study. 1671 68

Our current understanding of the nature of cell death that is associated with fatal organophosphate poisoning and the underlying cellular mechanisms is surprisingly limited. Taking advantage of the absence in an in vitro system of acetylcholinesterase, the pharmacological target of organophosphate compounds, the present study evaluated the hypothesis that the repertoire of cholinergic receptor-independent cellular events that underlie fatal organophosphate poisoning entails induction of mitochondrial dysfunction, followed by bioenergetic failure that leads to necrotic cell death because of ATP depletion. Pheochromocytoma PC12 cells incubated with the organophosphate pesticide mevinphos (0.4 or 4mumol) for 1 or 3h underwent a dose-related and time-dependent loss of cell viability that was not reversed by muscarinic (atropine) or nicotinic (mecamylamine) blockade. This was accompanied by depressed NADH cytochrome c reductase, succinate cytochrome c reductase or cytochrome c oxidase activity in the mitochondrial respiratory chain, reduced mitochondrial transmembrane potential, decreased ATP concentration, elevated ADP/ATP ratio, increased lactate dehydrogenase release and necrotic cell death. We conclude that Mev induces cholinergic receptor-independent necrotic cell death by depressing the activity of Complexes I to IV in the mitochondrial respiratory chain, eliciting reduction in mitochondrial transmembrane potential, depleting intracellular ATP contents and damaging cell membrane integrity.
...
PMID:Cholinergic-receptor-independent dysfunction of mitochondrial respiratory chain enzymes, reduced mitochondrial transmembrane potential and ATP depletion underlie necrotic cell death induced by the organophosphate poison mevinphos. 1698 2


<< Previous 1 2 3 4 5 6 Next >>

---