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)

In a cell-free system containing isolated nuclei and microsomal-cytoplasmic brain fraction there takes place a spontaneous puromycin-sensitive increase in acetylcholinesterase (AChE) activity of microsomes. As a result of preincubating the system with acetylcholine (ACh) (10(-6)-10(-3) M), AChE activity of microsomes was found to be increased, reaching the maximal value at an ACh concentration of 10(-5) M (25% during 60 min incubation). The effect of ACh was not detectable in the presence of actinomycin D and puromycin. Upon removal of the nuclei from the system, preincubation with ACh produces a lowering of AChE activity in microsomes. cAMP and cGMP reduce AChE activity of microsomes in a complete system. The results obtained enable one to consider acetylcholine regulation of microsomal AChE level in nerve cells as a multi-component system. The main component in the system is a direct action of ACh on the synthesis of AChE gene product or on its processing, while the other components (cyclic nucleotides and effect of ACh itself on translation) are elements of correction.
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PMID:[Regulation of acetylcholinesterase level in microsomes of neurons by acetylcholine and cyclic nucleotides]. 627 8

The possible functions of ornithine decarboxylase (ODC) and polyamines in the differentiation of mouse NB-15 neuroblastoma cells were investigated by examining the changes of these parameters in the differentiating and nondifferentiating NB-15 cells over a 5-day culture period. Differentiation of NB-15 cells was induced by the addition of dibutyryl cyclic AMP and 3-isobutyl-1-methylxanthine (1BMX) to the growth medium and was monitored by neurite outgrowth, increases of acetylcholinesterase (AChE), and RI cAMP-binding protein. Plating of NB-15 cells in fresh serum-containing growth medium was accompanied by rapid growth and a marked increase of ODC activity; this early increase of ODC activity was attenuated, both in duration and in magnitude, in the differentiating cells. The spermidine content of the differentiating neuroblastoma cells was significantly lower than that of the nondifferentiating cells. In the fully differentiated neuroblastoma cells, the ODC activity and spermidine content were lower than that of the undifferentiated cells by approximately 15-fold and five-fold, respectively. Based on these results it is proposed that changes of polyamine metabolism may be of significance in the differentiation of mouse neuroblastoma cells.
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PMID:Changes of ornithine decarboxylase activity and polyamine content upon differentiation of mouse NB-15 neuroblastoma cells. 628 99

The subcellular localization of calmodulin, cyclic nucleotide phosphodiesterase, and adenylate cyclase was studied in bovine adrenal medulla. Approximately 70% of the calmodulin and 90% of the cAMP phosphodiesterase activities were found colocalized in the cytoplasm. The subcellular distribution of adenylate cyclase closely paralleled the distribution of acetylcholinesterase, a marker for plasma membranes. The fraction of calmodulin which is particulate in nature has a distribution profile very similar to that of adenylate cyclase. The chromaffin granule fraction contained only 0.86% of the total cAMP phosphodiesterase, 0.41% of the total adenylate cyclase, and 1.4% of the total calmodulin.
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PMID:The subcellular localization of calmodulin, cyclic AMP phosphodiesterase, and adenylate cyclase in bovine adrenal medulla. 630 21

(R, S)-alpha-Fluoromethylornithine (alpha-FMO), a catalytic irreversible inhibitor of ornithine decarboxylase (L-ornithine carboxy-lyase, EC 4.1.1.17), induced the differentiation of N2a mouse neuroblastoma cells. The effect of alpha-FMO was concentration dependent; approximately 50% of the cell population exhibited neurite outgrowth in the presence of 1 mM alpha-FMO, while higher concentrations caused severe growth inhibition and cell death. The effect of 1 mM alpha-FMO on neuroblastoma differentiation was potentiated greatly by 0.1 to 0.2 mM N6,O2'-dibutyryl adenosine cyclic 3':5'-monophosphate (Bt2cAMP) causing more than 90% of the cell population to differentiate morphologically with thick and long processes; 0.1 to 0.2 mM Bt2cAMP, by itself, had no effect on cell growth and did not induce neurite outgrowth. The effect of alpha-FMO, either by itself or in combination with 0.1 to 0.2 mM Bt2cAMP, on the morphological differentiation of mouse neuroblastoma cells was reversed by the addition of exogenous putrescine or spermidine. The morphological differentiation of mouse neuroblastoma cells induced by 1 mM alpha-FMO plus 0.2 mM Bt2cAMP was accompanied by increases of the regulatory subunit of the type I cAMP-binding protein and acetylcholinesterase activity. These results indicate that the modulation of cellular polyamine contents may be important in neuroblastoma cell differentiation.
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PMID:Effects of inhibitors of ornithine decarboxylase on the differentiation of mouse neuroblastoma cells. 630 69

The concurrent localization of cyclic nucleotide immunofluorescent cells and acetylcholinesterase-containing neurons in the rat caudate-putamen complex has been examined. Cyclic AMP and cyclic GMP stained elements do not exhibit coincident localization with the enzymatically detectable hydrolysis of acetylcholine. These data add further support for the preferential association of the cyclic nucleotides with striatal efferent projection systems, while the large cholinergic somata are part of the interneuron population of the rat caudate-putamen complex.
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PMID:Rat striatal cyclic nucleotide-reactive cells and acetylcholinesterase reactive interneurons are separate populations. 632 52

Choline, acetylcholine and betaine used as a sole carbon source, effectuate in Ps. aeruginosa an acid phosphatase activity in addition to a cholinesterase activity. Induction of both enzyme activities was repressed by succinate or glucose. Cyclic AMP failed to relieve the repression produced by these compounds. Substrates not related to choline and used as a sole source of carbon, were inefficient to produce induction of both enzymes. The in-vitro action of choline, acetylcholine and betaine on Ps. aeruginosa acid phosphatase and cholinesterase has also been studied. To perform these studies periplasmic extracts obtained by EDTA-lysozyme treatment of the cells grown on choline or betaine as sole source of carbon, were used. Acid phosphatase activity was competitively inhibited by betaine, whereas the inhibition produced by choline and acetylcholine showed competitive and noncompetitive components. Cholinesterase activity was noncompetitively inhibited by betaine. At low acetylthiocholine concentration choline was an inhibitor of cholinesterase, whereas at high substrate concentration choline raised the hydrolysis rate of acetylthiocholine. These findings allow the conclusion that acid phosphatase and cholinesterase are specifically induced by choline and its metabolites derivatives. Kinetic results led us to postulate that acid phosphatase and cholinesterase contain a similar allosteric site. This site would either be of an anionic nature or show affinity to a methyl group or display both characteristics.
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PMID:Induction of acid phosphatase and cholinesterase activities in Ps. aeruginosa and their in-vitro control by choline, acetylcholine and betaine. 640 29

Studies are elaborated on regulation of acetylcholinesterase activity by nerve growth factor (NGF) in cultures of clonal PC12 pheochromocytoma cells. Acetylcholinesterase specific activity in these cultures is maximally and half-maximally increased by NGF concentrations of approximately 1-1.5 and 0.5 nM, respectively. These increases are blocked by antiserum to NGF and are neither mimicked nor significantly altered by epidermal growth factor (1-1000 ng/ml), dexamethasone (10 microM), or dibutyryl cAMP (1 mM). The action of NGF on acetylcholinesterase activity is abolished by low concentrations of the inhibitors of RNA synthesis, camptothecin and actinomycin D. Such findings indicate a transcriptional requirement for this effect of NGF. A series of PC12 variants were employed that in serum-containing medium do not show normal PC12 responses to NGF such as cessation of proliferation and neurite outgrowth. Each of the variants exhibited NGF-dependent increases in acetylcholinesterase specific activity. This suggests that the effects of NGF on regulation of acetylcholinesterase activity can be dissociated from the effects of the factor on neurite outgrowth and proliferation, and that NGF may therefore work via parallel or branching pathways.
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PMID:Regulation of acetylcholinesterase activity by nerve growth factor. Role of transcription and dissociation from effects on proliferation and neurite outgrowth. 724 Feb 10

The effects of the abnormal innervation in Hirschsprung's disease on colonic ion transport were examined in vitro using Ussing chambers. The response of the mucosal/submucosal preparations to different secretagogues were investigated in aganglionic and ganglionic rectosigmoid and transverse colon from children with Hirschsprung's disease and compared with normally innervated colon from children with anorectal anomalies. Basal values were similar in aganglionic and ganglionic rectosigmoid colon. Neurally mediated secretion with iloprost (10(-6) M) and acetylcholine (900 and 9 microM) was considerably reduced in aganglionic colon compared with normally innervated ganglionic colon. The ganglionic colon proximal to the aganglionic colon also had a reduced response to acetylcholine despite a normal acetylcholinesterase staining pattern. The responses to Escherichia coli STa enterotoxin (50 MU/ml) and isobutylmethylxanthine (10(-3) M) were similar in ganglionic and aganglionic colon. The response to STa enterotoxin was not changed by the nerve blocking agent tetrodotoxin (10(-6) M). The data show that colonocytes from aganglionic colon are capable of a normal secretory response if stimulated directly by cAMP or cGMP acting secretagogues but secretion in response to neurally mediated secretagogues is impaired. The hypertrophied acetylcholinesterase positive nerve fibres that infiltrate the aganglionic colon are likely to contribute to the reduced secretion to acetylcholine.
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PMID:Electrogenic colonic ion transport in Hirschsprung's disease: reduced secretion to the neural secretagogues acetylcholine and iloprost. 769 88

We found depolarization-dependent promotion of survival of cultured basal forebrain cholinergic neurons from postnatal 2-week-old rats. Over 30 mM KCl (high K+) as well as nerve growth factor (NGF) induced considerably high choline acetyltransferase (ChAT) activity and the increase was potentiated by the addition of BAY K8644, a Ca2+ channel agonist. The increase in ChAT activity by high K+ was due to the increased number of viable acetylcholinesterase-positive and ChAT-positive neurons. Also, a cyclic AMP analog gave the same effect as high K+, but its ability to induce the ChAT activity was higher than that of high K+. On the other hand, both high K+ and NGF had very little effects on the survival of the cultured cholinergic neurons from 10-week-old rats. Cyclic AMP analog induced considerable increase in ChAT activity and promotion of survival of cholinergic neurons in the 10-week-old culture. These findings showed that the neuronal death occurring just of the end of synapse formation in rat basal forebrain cholinergic neurons could be prevented by NGF and high K+, but the death of older cholinergic neurons could not. We propose the possibility that the death of postnatal 2-week-old basal forebrain cholinergic neurons in culture might be programmed cell death.
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PMID:High potassium and cyclic AMP analog promote neuronal survival of basal forebrain cholinergic neurons in culture from postnatal 2-week-old rats. 781 43

Porcine fetal lateral ganglionic eminence cells were transplanted into the quinolinic-acid-lesioned corpus striatum of immunosuppressed adult rats. The resulting grafts were analyzed for graft development with respect to donor age, donor cell dosage, and survival time from 5 to 22 weeks postimplantation. Graft development is prolonged by a factor of 3-4 times in porcine xenografts as compared to rat allografts. As grafts matured, neuronal somata developed in clusters that expressed acetylcholinesterase (AChE), tyrosine hydroxylase, and dopamine- and cAMP-associated phosphoprotein. These clusters were interspersed with AChE-poor graft regions consisting of small densely packed cells that stained for glial fibrillary acidic protein and porcine cluster of differentiation factor 44 (a species-specific glial marker). Graft axons could be selectively stained for 70-kDa neurofilament and were preferentially associated with AChE-poor, glial-rich regions in younger grafts (8 weeks), but AChE-rich neuronal regions in older grafts (22 weeks). Both graft axons and graft glial fibers projected for long distances into the host internal capsule, external capsule, corpus callosum, and anterior commissure. Donor axons also innervated host target structures including the globus pallidus and substantia nigra. This demonstrates a prolonged development of striatal cells that is appropriate to the donor species and which produces long-distance target-specific axonal growth within the adult host brain.
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PMID:Cytoarchitectonic development, axon-glia relationships, and long distance axon growth of porcine striatal xenografts in rats. 782 91


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