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)

Choline acetyltransferase (Ach-T) and acetylcholinesterase (Ach-E) activities in mice brain during the reverse action by imipramine, pheniprazine and pargyline to the syndrome elicited by intraperitoneal administration of Ro 4--1284 were investigated. A single dose of imipramine did not reverse reserpine-like syndrome whereas inhibited Ach-E activity and increased Ach-T activity at the same time. The reversal of reserpine-like syndrome by administration of pargyline, pheniprazine or chronic administration of imipramine was accompanied by no changes in Ach-E and Ach-T activities.
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PMID:Choline acetyltransferase and acetylcholinesterase activities in mice brain during the antagonistic action of antidepressant drugs and Ro 4--1284. 2 25

The variations of the time constant tau of the end-plate current (epc) have been studied at the clamped neuromuscular junction of the frog while transmitter release was focalised by local iontophoretic application of Ca++. In the absence of any anticholinesterasic drug, tau varies according to the variations of the intensity of epc (Iepc) due to pre or postsynaptic experimental procedure. It is suggested that focalisation of transmitter release induces local acetylcholinesterase inhibition by an excess of substrate; then the transmitter life time in the synaptic cleft is momentarily increased, allowing repeated binding of Ach to postsynaptic receptors.
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PMID:[Variation of the time constant (tau) of the decay of end-plate current during focalized transmitter release]. 40 28

We have devised a simultaneous assay system for megakaryocyte colony-stimulating factor (Meg-CSF) and megakaryocyte potentiator (Meg-Pot) by modifying a quantitative measuring technique for acetylcholinesterase activity (Ach-E) of megakaryocytes by automatic colorimetry using microplates. We cultured murine bone marrow cells treated with diisopropyl fluorophosphate in a serum-free system with serum-free pokeweek mitogen-stimulated spleen cell conditioned medium (PWM-SCM) and an unknown factor, preparing two microplates with the identical culture system. In the first plate, the total number of Ach-E-positive cells induced solely by the factor tested was indicative of Meg-CSF activity and additive increases in this parameter on simultaneous addition of PWM-SCM and the factor tested were indicative of early Meg-Pot activity. Total Ach-E activity (total change at optical density of 414 nm) per well was measured in the second plate to calculate total change at optical density of 414 nm per megakaryocyte, an indicator of late Meg-Pot activity. With this system, recombinant human erythropoietin showed both Meg-CSF and early and late Meg-Pot activities in in vitro megakaryopoiesis. Recombinant murine granulocyte-macrophage colony-stimulating factor possessed weak Meg-CSF and early Meg-Pot activity, whereas recombinant human granulocyte colony-stimulating factor exhibited late Meg-Pot activity and thrombocytopenic serum exhibited early and late Meg-Pot activities. This assay system is useful in screening Meg-CSF or Meg-Pot activities in unknown factors.
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PMID:Simultaneous assay for megakaryocyte colony-stimulating factor and megakaryocyte potentiator and its application. 169 13

Morphological changes and acetylcholinesterase (AchE) activity in the neuromuscular junctions (NMJ) of the normal and denervated posterior cricoarytenoid muscle (PCA muscle) of the cat were studied. Two days after denervation, the nerve terminals at the NMJ had almost disappeared. Six weeks after denervation, intensity of AchE activity at the former junctional site (FJS) was unchanged histochemically. At this stage, primary synaptic clefts were distorted and the Schwann's cells covered the FJS. Fourteen weeks after denervation, AchE activity at the FJS had decreased in contrast to that of the non-affected side. Calcitonin gene-related peptide (CGRP) was also investigated at the NMJ of the normal PCA muscles immunocytochemically. The present study shows that CGRP coexists with Ach in the nerve terminals of the PCA muscles and may be involved in the regulation of the contractile function of the intrinsic laryngeal muscle.
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PMID:Ultrastructural and histochemical study of the neuromuscular junctions in the denervated intrinsic laryngeal muscle of the cat. 188 87

The effects of three irreversible anticholinesterase agents, echothiophate (217MI), tertiary methylamine analog of 217MI (217AO) and Tetram, on end plate currents (e.p.c.s) of Rana pipiens cutaneous pectoris muscle were studied using electrophysiological techniques. All three compounds (217MI, 1-10 microM; 217AO, 1-25 microM; and Tetram, 1-50 microM) decreased the rate of e.p.c. decay (alpha) to the same extent as neostigmine (10 microM), a reversible anticholinesterase agent. Decay remained a single exponential at all membrane potentials. 217MI and its derivatives greatly reduced the normal voltage dependence of alpha represented by the slope (H = mV-1) of log alpha vs. membrane potential, in contrast to neostigmine which had no effect on H. Suppression of Ach release by the addition of 4 mM Mg++ to end-plates did not alter the reduction of H by 217AO indicating that the anticholinesterase-induced decrease in H is not simply due to an increased interaction between Ach and its receptors. Additionally, the pretreatment of end-plates with methanesulfonyl fluoride, also an irreversible cholinesterase agent, did not modify the effects of 217AO and Tetram on H. 217MI and its derivatives, at low concentrations which altered H, did not affect [3H]PCP or [125I]alpha-bungarotoxin binding to Torpedo californica Ach receptor-rich membranes. It is concluded that these agents alter H by an effect on the Ach receptor ion channel complex unrelated to either esterase inhibition or channel block.
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PMID:Echothiophate and cogeners decrease the voltage dependence of end-plate current decay in frog skeletal muscle. 248 Oct 33

The effects of hemicholinium-3 (HC-3) on spatial discrimination learning were studied. Rats were equipped with indwelling cannulae in the right lateral ventricle and, following recovery, were trained on a two platform spatial discrimination task in a water maze. In this task a visible escape platform remains in a fixed position in the pool during a single training session, whilst the location of an identical "float" (which affords no escape) is randomly varied. For each session the location of the fixed escape platform was changed and the rats were retrained to criterion following pretreatment either with artificial cerebrospinal fluid (CSF) or HC-3 (2.5, 5.0 micrograms/rat/ICV) 1 h before training. Each rat received every treatment according to a latin square design. The results showed that spatial learning was dose dependently impaired by HC-3, choice accuracy being reduced to chance levels by the higher dose. There was no evidence of motoric difficulty, as choice latencies were not significantly increased. Experiments were then conducted to test for reversal of the deficit using a range of psychotropic drugs. Rats were treated with CSF or HC-3 (5 micrograms/rat ICV) 60 min prior to testing and test drugs were injected 15 min before testing. Some doses of physostigmine (46-460 micrograms/kg/SC) and tetrahydroaminoacridine (THA) (2.2-10 mg/kg/SC) reversed the spatial learning deficit. The muscarinic agonists arecoline (0.046-1 mg/kg/SC), aceclidine (1-10 mg/kg/SC), oxotremorine (30-100 micrograms/kg/SC) and RS-86 (0.46, 1.0 microgram/kg/SC) were also effective. Pilocarpine (0.22-2.2 mg/kg/SC) showed marginal activity and isoarecoline (4.6-10 mg/kg/SC) was inactive. Nicotine (0.32, 1, 3.2 mg/kg/SC) and piracetam (10, 30, 100 mg/kg IP) were also inactive. The alpha 2 agonist, clonidine (46, 100 micrograms/kg SC) and the antagonist idazoxan (32, 100 micrograms/kg SC) were also inactive. Learning deficits were not reversed by haloperidol (20, 60 micrograms/kg), amphetamine (0.1, 0.46 mg/kg), the selective 5-HT1A agonist 8-OH-DPAT (30, 100 micrograms/kg) or by the benzodiazapine antagonist ZK-93426 (1, 3.2, 10 mg/kg). The results show that forebrain Ach depletion by HC-3 impairs spatial discrimination learning and these deficits are reversed by cholinesterase inhibitors and some muscarinic receptor agonists. Some degree of pharmacological selectivity is indicated by the failure of a range of other drugs to reverse the impairments.
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PMID:Hemicholinium-3 impairs spatial learning and the deficit is reversed by cholinomimetics. 252 45

Intrastriatal injection of soman (14.85 nmol) inhibits cholinesterase (ChE) activity in the striatum with much smaller decreases in ChE activity in other brain areas of the rat. As would be expected, there is a substantial increase in striatal acetylcholine (ACh) content shortly after soman injection. However, this increase is no longer significant 1 h following intrastriatal injection. There is no change in striatal KACh 20 min, 1 h or 24 h following soman injection. ACh content is not affected in the parietal cortex, hippocampus, or medulla/pons following intrastriatal soman injection. However, KACh and/or ACh turnover are reduced in these brain areas following soman injection. There is no consistent effect on dopamine (DA) metabolism in any of the brain areas studied. However, serotonin (5-HT) metabolism appears to be affected in the cortex, hippocampus and medulla/pons following intrastriatal injection of soman. Possible mechanisms of the actions of local injection of soman on brain Ach and 5-HT metabolism are discussed, as well as the differences observed between the effects of local and peripheral administration of soman on DA metabolism in the striatum.
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PMID:Effect of intrastriatal injection of soman on acetylcholine, dopamine and serotonin metabolism. 337 62

In the lichen Parmelia caperata (L.) Ach. the distribution pattern of membrane-bound Ca2+ is investigated in the symbionts by chlorotetracycline (CTC)-induced fluorescence during the development of propagative structures, the soredia. The results demonstrate that Ca2+ accumulation in the alga and the fungus is associated with this morphogenetic process; particularly, polarized hyphal growth involves a tip-to-base Ca2+ gradient. CTC fluorescence distribution is coincident with that of cholinesterase (ChE) activity during morphogenesis of soredia. A comparison is suggested with 'embryonic ChE' of animal cells, where developmental events are regulated by a cholinergic mechanism that also modulates Ca2+ levels.
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PMID:Membrane-bound Ca2+ distribution visualized by chlorotetracycline fluorescence during morphogenesis of soredia in a lichen. 339

We studied the effects of recombinant erythropoietin (r-Epo) and thrombocytopenic serum (TS) on the cytoplasmic maturation of megakaryocytes derived from colony-forming units megakaryocyte (CFU-M). Serotonin content, ATP content, acetylcholinesterase (Ach-E) activity per megakaryocyte, and electron microscopic analysis were selected as markers of cytoplasmic maturation. Megakaryocytes induced by pokeweed mitogen-stimulated spleen cell-conditioned medium (PWM-SCM) alone showed low levels of ATP content and Ach-E activity, which did not increase during culture, as well as a low level of serotonin content, which gradually accumulated during day 7 of culture. When r-EPo was added to the culture system on day 3 after megakaryocytic colony formation with PWM-SCM, the serotonin content in megakaryocytes increased markedly but ATP content and Ach-E activity did not increase significantly. In contrast, TS caused an increase in ATP content and Ach-E activity, but did not cause an increase in serotonin content. Electron microscopic analysis showed that the demarcation membrane system (DMS) developed defectively only in local areas with the addition of r-Epo and PWM-SCM, whereas the DMS developed normally and dense granules were generated to near normal with the addition of TS. Recombinant Epo may act on the early stage of cytoplasmic maturation, whereas TS may act on the late stage of cytoplasmic maturation. The results shown herein suggest that at least two different factors may be necessary for full in vitro cytoplasmic maturation of megakaryocytes derived from CFU-M.
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PMID:In vitro regulatory mechanisms for cytoplasmic maturation of murine megakaryocytes derived from colony-forming units megakaryocyte (CFU-M). 340 56

Membrane acetylcholinesterase activity is considered to be a marker for a cholinergic system. When temporarily expressed in differentiating cells other than the nervous or muscular ones, it may play a role in morphogenesis. In the lichen Parmelia caperata (L.) Ach., acetylcholinesterase is histochemically localized mainly in the cell walls and/or membranes of both symbionts just where they proliferate and form well-organized propagation structures, the soredia. The enzyme activity is first detected in a few algae undergoing aplanosporogenesis and later in medullary hyphae that reach the dividing algae by elongating perpendicularly to the thallus surface. This histochemical pattern that is associated with algal proliferation and oriented hyphal growth is characteristic of early morphogenesis of the soredia; when fully differentiated, they consist of an inner dividing alga and an outer hyphal envelope, both showing cholinesterase activity. Substrate specificity and inhibitor sensitivity of the histochemical staining indicate an acetylcholinesterase-like activity. However, extracts of the thallus areas where soredia develop give four bands of cholinesterase activity on disc electrophoresis: the two cathodal bands have the characteristics of acetylcholinesterase, the others of pseudocholinesterase. One of the latter hydrolyses propionylthiocholine very rapidly. The findings suggest that in lichen symbiosis, a cholinergic-like system participates in regulating morphogenetic processes such as cell division, oriented tip growth and alga-fungus membrane interactions. Environmental stimuli, particularly light, might trigger the development of soredia by modulating the activity of the cholinergic mechanism.
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PMID:Preliminary evidence for a cholinergic-like system in lichen morphogenesis. 355 3


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