Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myoblasts from rudiments of slow and fast muscle, anterior latissimus dorsi (ALD) and posterior latissimus dorsi (PLD) respectively, of 9-day-old quail embryos were cultured in vitro for a period of up to 60 days in order to give rise to well-differentiated muscle fibres. These fibres were innervated by neurons from either quail or mouse embryo spinal cord and their innervation pattern was examined by the visualization of acetylcholine receptors (ACh-R) and of acetylcholinesterase (ACh-E) activity at the neuromuscular contacts. In the culture system used, quail neurons always innervated muscle fibres at several sites and only when a fast-type activity was imposed on these neurons did a reduction in the number of the previously established neuromuscular contacts take place. In contrast, in the muscle fibres innervated by mouse neurons, a spontaneous reduction in the number of the previously established neuromuscular contacts occurred but this spontaneous reduction depended upon the level of differentiation reached by the muscle fibres in vitro. In the cultures of muscle fibres previously innervated by mouse neurons, the addition of quail neurons did not provoke any modification in the initial innervation pattern, and no quail ACh-R cluster was observed. In contrast, in the muscle fibres previously innervated by quail neurons, the mouse neurons contacted these fibres, resulting in a decrease in the number of quail ACh-R clusters. These results emphasize the part played by neurons in the establishment of the innervation pattern when muscle fibres have reached a high level of differentiation. In vitro, the slow and fast characteristics of the muscle fibres do not influence this pattern.
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PMID:In vitro regulation of the innervation pattern of quail muscle fibers by quail and mouse neurons. 162 60

1. Acetylcholine (ACh), 7.5 x 10(-5) M, and carbachol, 5 x 10(-6) M (CCh) depressed the frequency of miniature endplate potentials (m.e.p.ps) in the frog (Rana temporaria) sartorius neuromuscular junction with active acetylcholinesterase to about 50-55% of the controls. 2. A similar depression was produced by the nicotinic agonists, nicotine, suberyldicholine and tetramethylammonium. 3. The muscarinic agonists, oxotremorine, methylfurmethide and methacholine were without effect on m.e.p.p. frequency. The muscarinic antagonist, atropine and the nicotinic antagonist, (+)-tubocurarine, had no effect on the depression of m.e.p.p. frequency evoked by CCh. 4. The ganglionic blockers, benzhexonium and IEM-1119, were also without effect on the CCh-evoked depression of m.e.p.p. frequency. 5. Pretreatment of muscles with anticholinesterases did not prevent the CCh-induced drop in m.e.p.p. frequency. 6. The effect of CCh was proportionally the same as in the controls in preparations where the m.e.p.p. frequency was changed by elevation of K+ and in the presence of theophylline, noradrenaline, dibutyryl adenosine 3':5'-cyclic monophosphate (db cyclic AMP) and db cyclic GMP. 7. An inhibitor of Na+,K(+)-ATPase, ouabain, 5 x 10(-5) mol l-1, prevented or reversed the depression of m.e.p.p. frequency by CCh. However, the depression was present in a nominally K(+)-free medium. Insulin and adrenaline, which are considered to be Na+,K(+)-ATPase activators, were without effect on depression of m.e.p.p. frequency. 8. The depression of m.e.p.p. frequency by 5 x 10(-6) M CCh was the same at temperatures between 5 and 30 degrees C with a Q10 near to 1.0. When threshold amounts of CCh were used (6 x 10-7 and 3 x 10-7 M), the depression was less at higher temperatures.9. The receptive structures responsible for the CCh (or ACh)-evoked depression of m.e.p.p. frequency differ pharmacologically from muscarinic, nicotinic ganglionic and neuromuscular junction ACh-receptors as well as from the synaptic cholinesterase, in contrast to previous reports (Duncan & Publicover, 1979).The low temperature-dependence points to the possibility that physical rather than biochemical processes are limiting in this presynaptic effect of cholinomimetics.
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PMID:Depression of miniature endplate potential frequency by acetylcholine and its analogues in frog. 166 83

1. Acetylcholine reduced atrial contractions by 82.5% in guinea pig, 50.8% in rat, and 41.5% in rabbit. 2. The EC50 values for the negative inotropic effect of acetylcholine were 3.3 x 10(-7) M in rat and guinea pig atria and 4.1 x 10(-6) M in rabbit atria. 3. There was no correlation between the species differences in the negative inotropic effect of acetylcholine in atria and the density or affinity of acetylcholinesterase or muscarinic receptors. 4. Inhibition of atrial acetylcholinesterase with soman reduced the EC50 of acetylcholine three-fold in all species, but did not change the maximal inotropic effect of acetylcholine. 5. Species differences in the negative inotropic effect of acetylcholine may be caused by differences in the coupling between myocardial muscarinic receptors and the ion channels that mediate negative inotropy.
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PMID:Species differences in the negative inotropic effect of acetylcholine and soman in rat, guinea pig, and rabbit hearts. 168 57

A sensitive enzymatic assay to measure cholinesterase activity in serum using liquid chromatography with electrochemical detection has been devised and used to examine cholinesterase inhibition in mice treated with diisopropyl phosphorofluoridate. Acetylcholine was used as substrate, and a postcolumn reactor containing immobilized choline oxidase converted the enzymatic product, choline, and the internal standard, ethylhomocholine, into the electrochemically active H2O2. The postcolumn reactor also contained acetylcholinesterase to allow the indirect detection of the substrate. Assay optimization included investigations of substrate concentration, buffer pH and ionic strength, enzyme concentration, incubation time, and reaction termination method. The optimized procedure is applicable to samples with activities of 0.11 to 269 mmol/ml/h. Intrasample coefficient of variation for mouse serum samples was 1.7% (n = 12), while intersample coefficient of variation was 8.0% (n = 5). The mean +/- SE serum cholinesterase activity found for controls and mice treated with diisopropyl phosphofluoridate (6.3 mg/kg, ip, 24 h prior) was 158.7 +/- 5.7 mumol/ml/h and 36.6 +/- 3.1 mumol/ml/h, respectively (P less than 0.001).
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PMID:Determination of serum cholinesterase activity by liquid chromatography with electrochemical detection. 177 88

A simple method for the separate determination of acetylcholinesterase and butyrylcholinesterase activities in amniotic fluid is reported. This determination is performed with an enzyme electrode involving an immobilized choline oxidase membrane associated with the amperometric detection of hydrogen peroxide. Acetylcholine or butyrylcholine, in the presence of samples containing acetylcholinesterase or butyrylcholinesterase are specifically hydrolyzed, the formation of choline being detected vs time by the sensor with no need for a selective inhibitor. The dynamic linear ranges for acetylcholinesterase and butyrylcholinesterase are respectively 100 microU to 10 mU and 30 microU to 3 mU per ml sample.
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PMID:Rapid and sensitive discriminating determination of acetylcholinesterase activity in amniotic fluid with a choline sensor. 177 89

Different regions of the prostate gland, namely the prostatic capsule, peripheral prostate, and proximal and distal central prostate, were obtained from 5 patients with carcinoma of the bladder and studied histochemically and immunohistochemically to localise acetylcholinesterase (AChE)-, dopamine beta-hydroxylase (DBH)-, serotonin- and peptide-containing nerves. Autonomic ganglia were found in all regions of the prostate studied. The greatest number of ganglia contained AChE and neuropeptide Y (NPY) followed (in decreasing order) by DBH; [Met]enkephalin (mENK) and [Leu]enkephalin (IENK); calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP); and serotonin, but not somatostatin. The greatest density of nerve fibres was found in the proximal central prostate, followed by the anterior capsule and distal central prostate, with the least in the peripheral prostate. The greatest number of nerve fibres contained ACh and NPY, followed in decreasing order by VIP and DBH; IENK, serotonin and CGRP; mENK; substance P and somatostatin. The functions of the neurotransmitter substances in the human prostate remain to be elucidated.
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PMID:The human prostate gland: a histochemical and immunohistochemical study of neuropeptides, serotonin, dopamine beta-hydroxylase and acetylcholinesterase in autonomic nerves and ganglia. 187 92

This study sought to determine whether the choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) enzymes in the brain were affected in a regionally selective manner by chemical and physical stressors: 1) subacute administration of physostigmine (Phy); 2) exercise; and 3) the combination of these two stressors. ChAT and AChE activities in corpus striatum were significantly decreased due to Phy as well as Phy + exercise. This suggests that corpus striatum is affected by chemical stressors but more so by the combination of chemical and physical stressors. The brainstem is the only region which showed inhibition of ChAT activity due to exercise. Subacute Phy also inhibited brainstem ChAT activity. The hippocampus showed significant decrease in ChAT activity due to Phy + exercise but not due to Phy alone. These results suggest that the brain regions involved with control of motor, autonomic and cognitive functions were affected by subacute Phy and exercise. These data are consistent with the hypothesis that the responsiveness of these brain regions to different stressors is a function of the level of ongoing cholinergic activity and that elevations in ACh levels due to AChE inhibition may have long-term effects on the regulation of ChAT and AChE activities through a negative feedback mechanism.
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PMID:Effect of cholinesterase inhibitor and exercise on choline acetyltransferase and acetylcholinesterase activities in rat brain regions. 194 75

To obtain additional evidence in support of the co-transmitter role of glutamate in cortical cholinergic terminals proposed by Docherty et al., the right nucleus basalis in rats was lesioned with ibotenic acid; resulting changes in cortical acetylcholinesterase (AChE) staining, glutamate content, and the release of [3H]acetylcholine ([ 3H]ACh) and glutamate from cortical slices from the two sides were compared. While there was a profound reduction on the lesioned side in cortical AChE activity and in the size of the releasable pool of [3H]ACh, neither the content nor the evoked release of glutamate was reduced significantly on the lesioned side. Furthermore, while oxotremorine strongly depressed the evoked release of [3H]ACh, it had no effect on the evoked release of endogenous glutamate measured simultaneously. These results do not support the co-transmitter role of glutamate in cortical cholinergic terminals, although they cannot statistically exclude that a small fraction of glutamate has a co-transmitter role, as proposed by Docherty et al.
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PMID:Is glutamate a co-transmitter in cortical cholinergic terminals? Effects of nucleus basalis lesion and of presynaptic muscarinic agents. 197 43

In combination with transmission electron microscopy (TEM), histochemistry for acetylcholinesterase (AChE) and immunohistochemistry for vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY) were carried out on the intraepithelial nerve fibers of the guinea-pig nasal gland. AChE-positive nerve profiles and VIP-immunoreactive nerve profiles were detected in abundance within the epithelium of the glandular acini and within the epithelium of intralobular excretory ducts including the intercalated and striated ducts. Intraepithelial NPY-immunoreactive nerve profiles were also considerably large in number in the nasal gland, but less frequent than the other two types of nerve profiles; furthermore, the NPY-immunoreactive nerve profiles appeared absent within the epithelium of the striated duct. All the intraepithelial nerve varicosities were in close spatial contact with the epithelial cells of the acinus and the duct and also with the myoepithelial cells, which were commonly seen in the acinus and the intercalated duct. Throughout the present study, however, no membranous specializations could be found between the nerve varicosities and the epithelial cells or the myoepithelial cells. The present results suggest an intense and delicate regulation through the collaboration among ACh, VIP and NPY of the secretory activity of the guinea-pig nasal gland, including the emission of acinar secretions into the duct through contraction of the myoepithelium and modification of the secretion contents by the duct epithelium.
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PMID:An electron microscopic study of acetylcholinesterase-activity and vasoactive intestinal peptide- and neuro-peptide Y-immunoreactivity of the intraepithelial nerve fibers in the nasal gland of the guinea pig. 203 60

Acetylcholine (ACh) and acetylcholinesterase (AChE) are main components in cholinergic nervous system. ACh is a natural constituent of many parts of the nervous system and its chief role is neurotransmission. It is not entirely unique in function to the cholinergic tissues of the human body. Gingiva is the part of the oral mucosa which contains numerous mast cells. They contain a variety of biologically active substances including neurotransmitters such as 5-hydroxytryptamine, histamine etc. In the dental literature accessible to authors no data were found on ACh and AChE in the different oral structures in health and inflamed conditions. Therefore gingiva samples from 50 human individuals representing varying grades of inflammatory involvement have been utilised in the present study. ACh and AChE were estimated in the gingiva tissues by flurometric and spectrophotometric methods. This study established hithero unknown "norms" for the ACh and AChE contents of the clinically normal gingiva, which are found to be 0.85 +/- 0.06(SE) ug/g and 210 +/- 18(SE) micromoles ACh hydrolysed/hr/gm/wet tissues. Results also revealed that the range of variations of ACh is high and AChE is low in all the inflamed states of gingival tissues.
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PMID:Cholinergic components in human gingiva in healthy and inflamed states. 209 61


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