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 action of eserine of acetylcholinesterase (AchE) reversible inhibitor of frog muscle fibres membrane potential (MP) under various physico-chemical conditions in external solution was studied. The data obtained show that changes of external pH in any direction decrease the depolarisation of the membrane produced by eserine. The dose-effect curve is linear at pH 7, but it has saturation at pH 6 and pH 9. Dependence of the membrane depolarisation in the presence of eserine upon calcium ions concentration in external solution is S-shape. Protonophore 3C1CCP (carbonilcianamid-m-3C1-phenylhydrazon) depolarises the membrane further in the presence of eserine. Valinomycin under these conditions completely restores the MP. Evidence is obtained that eserine reduces potassium permeability of the muscle membrane. It is supposed that membrane-bound AchE is involved in the ionic permeability regulation of the muscle membrane at rest.
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PMID:[Eserine-induced change in membrane potential of frog muscle fibers]. 96 99

A new method for assaying endocytosis in erythrocyte ghosts is presented. The method involves measuring the percentage loss of acetylcholinesterase activity which occurs when vacuoles form, making the acetylcholinesterase on the vacuole surface inaccessible. This method is compared to other methods of measuring endocytosis in this system, including phase contrast microscope estimation of vesiculation, stereological analysis of electron micrographs to determine vesiculation and loss of sialic acid accessible to neuraminidase due to endocytosis. Comparison of the percentage loss of acetylcholinesterase activity with the electron micrographic and sialic acid methods showed that all three methods gave a quantitative measure of the percentage of total membrane area taken in as vesicles. Since the acetylcholinesterase method was fast, easy, inexpensive, and quantitative, it was the preferred method for assay of endocytosis. The inhibition of endocytosis by Ca2+ was observed with this method; the success of this experiment demonstrated the applicability of the method to the study of inhibitors of endocytosis.
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PMID:A new assay for endocytosis in erythrocyte ghosts based on loss of acetylcholinesterase activity. 98 35

1. Rabbit retinas were isolated and superfused with a physiological medium. Ganglion cell activity was recorded during stimulation with focused light, and receptive fields were mapped. Receptive fields were identical to those found in vivo and did not change during a 6-h incubation. After the receptive field of a ganglion cell had been identified, acetylcholine or related agents were introduced singly or in combination into the medium, and their effect on the cell's spontaneous and light-evoked activity was observed. 2. Ganglion cells with on-center or directionally selective receptive fields were excited when ACh was added to the medium. The response to exogenous ACh was prevented by cholinergic antagonists. 3. These cells' spontaneous activity and response to light were enhanced by anticholinesterase and depressed by cholinergic antagonists. Antagonists varied in their ability to block the light-evoked response, with dihydro-beta-erythroidine the most effective. 4. Thresholds for ACh or the related agents were low, ranging from 1 to 40 muM; their effects were rapidly and completely reversed when the retina was returned to control medium. 5. In retinas incubated in medium containing 20 mM Mg2+ and 0.2 mM Ca2+, ganglion cells lost completely both their spontaneous and light-evoked activity, but retained their ability to generate action potentials in response to elevated K+. Ganglion cell activity rapidly returned to normal when the retina was returned to medium containing normal electrolytes. On-center and directionally selective cells were excited by ACh in retinas where synaptic transmission had been inhibited by 20 mM Mg2+ and 0.2 mM Ca2+. 6. The responses of on-center and directionally selective cells to ACh, to anticholinesterase, and to cholinergic antagonists in control medium indicate that the retina contains one or more synapses using ACh as a neurotransmitter. The response to ACh in retinas exposed to 20 mM Mg2+ and 0.2 mM Ca2+ suggests that at least one such synapse in on the ganglion cell itself. 7. Off-center cells were inhomogenous in their response to ACh. Although some responded just as the other classes of cell, the majority responded quite weakly and a subgroup was encountered which was entirely unaffected by even 1 mM ACh, by levels of physostigmine which inactivate virtually all retinal acetyl-cholinesterase, or by high concentrations of cholinergic antagonists. Only 2 of 20 off-cells tested in the presence of 20 mM Mg2+ and 0.2 mM Ca2+ were excited by ACh. Apparently ACh is not a primary transmitter for most off-cells.
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PMID:Responses to acetylcholine of ganglion cells in an isolated mammalian retina. 99 29

The effects of treating adult wethers with 2 or 4 mg of coumaphos/kg of body weight each day for 6 days were investigated. The smaller dose produced a gradual decrease of erythrocyte acetylcholinesterase (AChE) activity (to maximum average reduction of approximately 45%), but without the appearance of signs of toxicosis. The larger dose appeared to be toxic. Treatment with the drug did not seem to alter significantly the anticholinesterase effects of a 2nd treatment made 6 weeks later. Coumaphos did not significantly affect serum activities of aspartate aminotransferase (glutamic oxalacetic transaminase) or isocitrate dehydrogenase (ICD) and concentrations of serum sodium and plasma calcium. A marked decrease in blood serum potassium and an increase in plasma magnesium occurred in all wethers that died after treatment with coumaphos, whereas appreciable changes did not occur in the survivors of the treatment given 6 weeks earlier. Treatment of sheep with an intravenous injection of the organophosphorous compound trichlorfon, insufficient to produce a significant effect on erythrocyte cholinesterase activity, produced additive effects with those of coumaphos.
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PMID:Repeated oral administration of coumaphos in sheep: effects on erythrocyte acetylcholinesterase and other constituents. 111 26

1. Longitudinal muscle strips of the guinea-pig ileum were incubated in Tyrode solution containing either DFP or physostigmine as cholinesterase inhibitor. After a 90 min preincubation period the acetylcholine resting release into the medium was determined. Acetylcholine was estimated by gas chromatography. 2. The resting release was 0.39 nmol/g times min irrespective of the cholinesterase inhibitor used. In the presence of hexamethonium, or after omission of external calcium, the resting release fell by 50 and 55 per cent, respectively. 3. Oxotremorine (10-5 and 10-4M) significantly inhibited the resting release of acetylcholine by 25 and 33 per cent, respectively. The inhibitory effect of oxotremorine was completely reversed by atropine (3 times 10-7 M). Oxotremorine did not reduce the spontaneous release of acetylcholine that occurred either in the presence of hexamethonium or in the absence of external calcium. 4. The acetylcholine content of the muscle strips was approximately doubled during the preincubation with a cholinesterase inhibitor. The subsequent incubation with oxotremorine did not lead to a further increase in the endogenous acetylcholine content. However, incubation of the muscle strips with oxotremorine in the absence of a cholinesterase inhibitor led to a rise in the endogenous acetycholine concentration. In in vivo experiments, oxotremorine also caused an increase in the acetylcholine content of the muscle strips. The possibility is discussed that the rise in the acetylcholine concentration following the administration of oxotremorine is a consequence of the decreased release. 5. It is concluded that oxotremorine inhibits the resting release of acetylcholine by activation of neuronal muscarinic receptors. The inhibitory effect of exotremorine is linked to that fraction of the acetylcholine resting release that is calcium-dependent and that arises from propagated activity in cholinergic neurones. The results are consistent with the hypothesis of a feed-back control of acetylcholine release mediated by inhibitory muscarinic receptors.
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PMID:Inhibition by oxotremorine of acetylcholine resting release from guinea pig-ileum longitudinal muscle strips. 111 41

Studies on the effect of chloroquine on frog's rectus abdominis muscle have been performed. Relatively low concentrations of chloroquine, 5 times 10-5 and 2 times 10-4 g/ml inhibited cholinesterase activity and potentiated acetylcholine (ACh)-induced contractions but antagonized carbachol and caffeine contractions, as well as ACh-induced contractions of eserinized muscle. High concentrations (5 times 10-4 and 2 times 10-3 g/ml) non-competitively antagonized contractions to ACh, carbachol, caffeine and potassium. It was suggested that the blocking action of chloroquine was due to its local anaesthetic property and interference with intracellular calcium movements.
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PMID:Dual action of chloroquine on frog's skeletal muscle contraction. 112 35

The transsynaptic induction of the monoamine transporter present on the membrane of chromaffin granules was studied in primary cultures of dissociated bovine adrenomedullary cells submitted to a chronic secretory stimulation. The amount of the vesicular monoamine transporter was assayed by binding of the specific ligand [3H]-dihydrotetrabenazine. After several days of incubation in the presence of high potassium, the concentration of [3H]-dihydrotetrabenazine binding sites was increased by a 1.5-2.5 factor. This increase was smaller in the presence of the cholinergic agonist carbachol. The long-term inductions of the vesicular monoamine transporter, of tyrosine hydroxylase, and of acetylcholinesterase were of similar magnitude. Under the same conditions, we found no variation in either the activities of other catecholamine biosynthetic enzymes (dopamine beta-hydroxylase and DOPA decarboxylase), or in metabolic enzymes such as lactate dehydrogenase and cytochrome c oxidase, and a decrease in the cellular content of chromogranin A and cytochrome b-561. The induction of the vesicular monoamine transporter was inhibited by the calcium channel antagonists, fluspirilene and nifedipine, and was increased by the agonist Bay K 8644. It was abolished by cycloheximide and actinomycin D. These results indicate that calcium entry into chromaffin cells increases the synthesis of the vesicular monoamine transporter, presumably by transcriptional activation. Elevation of intracellular cyclic AMP concentration or activation of protein kinase C also induced an increase in the expression of the vesicular monoamine transporter. Our results confirm that components of storage vesicle membranes are differentially regulated in response to secretory stimulation, as are several cytosolic or intravesicular soluble proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of the chromaffin granule catecholamine transporter in cultured bovine adrenal medullary cells: stimulus-biosynthesis coupling. 127 22

Four different oil-based diets were used in a feeding study involving rats to assess the relationship between the fatty acid composition of the dietary fat and its influence on erythrocyte membrane (EM) lipid composition and the activities of membrane-bound enzymes. Nutritionally adequate diets containing 20% groundnut (GNO), coconut (CO), safflower (SO), or mustard oil (MO) were fed to weanling CFY rats for 4 months. EMs were analyzed for total cholesterol, phospholipids, fatty acid profiles, and sialic acid content. Activities of membrane-bound enzymes such as Na+, K(+)-adenosine triphosphatase (ATPase), Mg(2+)-ATPase, Ca2+, Mg(2+)-ATPase, and acetylcholinesterase were also assayed. The activities of all membrane-bound enzymes, except Mg(2+)-ATPase, and sialic acid content were higher in the MO-fed group than in the rest of the groups. Ca2+, Mg(2+)-ATPase activity was distinctly lower in the SO-fed group than in the other groups. Cholesterol to phospholipid molar ratio was similar in all the groups. However, SO- and MO-fed groups displayed an increased cholesterol content and a higher degree of unsaturation in the membrane fatty acid composition. The higher membrane fatty acid unsaturation in the SO-fed group was principally due to linoleic (18:2) and arachidonic (20:4) acids, while in the MO-fed group it was mainly due to oleic (18:1), eicosenoic (20:1), erucic (22:1), and linoleic (18:2) acids. These results suggest a relationship between the quality of dietary fat, EM fatty acyl composition, and the activities of membrane-bound enzymes.
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PMID:Effect of dietary fats on erythrocyte membrane lipid composition and membrane-bound enzyme activities. 131 27

Unexpectedly, it was observed that the P2-purinoceptor antagonist, suramin (10 microM to 1 mM), reversed the muscle paralysis caused by structurally unrelated non-depolarizing relaxants. Suramin competitively reversed the blocking action of pancuronium. Both the pre- and postsynaptic blockade of nicotinic receptors by pancuronium was counteracted, as shown by the action of suramin, using train-of-four stimulation. Suramin did not affect the paralysis caused by the depolarizing relaxant, succinylcholine. The reversal action of suramin was not due to an increase in the acetylcholine concentration in the synaptic cleft, since neither the contraction of preparations partially paralysed by diminished acetylcholine release in the presence of low Ca2+ or high Mg2+ nor acetylcholinesterase activity were affected. Suramin did not affect the reduction in twitch tension caused by adenosine and potentiated the ATP-induced reduction in twitch, indicating that ATP-sensitive receptors are not involved in the reversal action of suramin. Consequently, these results suggest that the action of suramin is due to binding with a site on the acetylcholine receptor also occupied by non-depolarizing relaxants, but different from the site occupied by succinylcholine.
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PMID:Suramin reverses non-depolarizing neuromuscular blockade in rat diaphragm. 132 40

Neuromuscular transmission was studied in the rat phrenic nerve-hemidiaphragm preparation with acetylcholinesterase (AChE) partially inactivated. Enzyme inhibition resulted in (1) increased single-twitch tension of the diaphragm; (2) compound muscle action potential (CMAP) containing repetitive discharges; (3) stimulus-induced antidromic backfiring (SIAB) seen in the phrenic nerve; and (4) repetitive nerve stimulation (RNS) eliciting a decrement-increment (D-I) phenomenon (i.e., amplitude reduction maximal with the second CMAP). Using a high-calcium and low-magnesium solution, SIAB and the decrement of the second CMAP during RNS were intensified, whereas closely spaced trains and (+)-tubocurarine (TC) abolished SIAB and simultaneously prevented the decrement of the second CMAP. Importantly, low concentrations of (+)-TC prevented SIAB in the phrenic nerve, while the repetitive discharges of the CMAP and the increase in twitch tension remained unaffected. This observation suggests that preterminal nicotinic receptors stimulated by released acetylcholine induce SIAB, whereas postsynaptic events are less important in the generation of SIAB. SIAB, a presynaptic event, appears to be responsible for the transient impairment of the neuromuscular transmission, i.e., the D-I phenomenon.
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PMID:Impaired neuromuscular transmission during partial inhibition of acetylcholinesterase: the role of stimulus-induced antidromic backfiring in the generation of the decrement-increment phenomenon. 132 79


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