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 influence of dexamethasone on the development of neurons and oligodendrocytes was studied in serum-free, aggregating rat brain cell cultures. Synaptogenesis and myelination occur in this culture system. The concentration of myelin basic protein and the activity of 2',3'-cyclic nucleotide 3'-phosphodiesterase were used as oligodendroglia and myelin markers. Choline acetyltransferase and acetylcholinesterase served as neuronal markers, glutamine synthetase reflected astrocyte differentiation, while ornithine decarboxylase served as a general marker for cell growth and maturation. This study showed that dexamethasone stimulated the differentiation of cholinergic neurons and astrocytes. The effect of dexamethasone on oligodendroglial differentiation and myelination depended on the stage of development: during the early phase of myelination dexamethasone had a stimulatory effect, whereas at a later stage it showed a significant inhibition.
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PMID:Dexamethasone stimulates the biochemical differentiation of fetal forebrain cells in reaggregating cultures. 242 5

PC12 cells, which differentiate morphologically and biochemically into sympathetic neuron-like cells when treated with nerve growth factor, also respond to fibroblast growth factor. Some of the changes induced by fibroblast growth factor are similar to those seen after nerve growth factor treatment. Specifically, pituitary fibroblast growth factor causes the formation of processes initially comparable to those produced by nerve growth factor. However, in contrast to the outgrowth induced by nerve growth factor, which continues for several days, the outgrowth of processes induced by fibroblast growth factor ceases after about 3 days, even though fresh fibroblast growth factor is added. After about 6 days the processes induced by fibroblast growth factor have virtually disappeared. In this regard the processes induced by fibroblast growth factor are very similar to those induced by dibutyryl cyclic adenosine 3':5'-monophosphate (dBcAMP). The addition of nerve growth factor and fibroblast growth factor together appears to produce a synergistic effect on process formation, as does the simultaneous addition of nerve growth factor and dBcAMP. Cells pretreated (or primed) with nerve growth factor are able to regenerate processes much more rapidly in the presence of nerve growth factor than cells which have not been pretreated. When fibroblast growth factor is added to cells primed with nerve growth factor, more rapid regeneration of processes also occurs. The regeneration of neurites in response to either factor is blocked by the addition of an inhibitor of methylation. The process formation induced by fibroblast growth factor is preceded, as is the outgrowth in response to nerve growth factor treatment, by an induction of ornithine decarboxylase, a decrease in the phosphorylation of a specific cytoplasmic protein, and an increase in the phosphorylation of a specific non-histone nuclear protein. The effects of fibroblast growth factor and of nerve growth factor on ornithine decarboxylase are additive. Fibroblast growth factor does not cause an increase in the activity of acetylcholinesterase; nerve growth factor does. Fibroblast growth factor does not appear to be acting through the nerve growth factor receptor. The binding of iodinated nerve growth factor to PC12 cells is specific and is not inhibited by the presence of fibroblast growth factor. In addition, anti-nerve growth factor serum does not interfere with the action of fibroblast growth factor.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effect of fibroblast growth factor on PC12 cells. 298 39

We have identified a new subline of PC12 pheochromocytoma cells (PC12D cells) in which neurites are extended within 24 hr in response to cAMP-enhancing reagents as well as in response to nerve growth factor (NGF), but not in response to epidermal growth factor or phorbol diester. Anti-NGF antiserum did not affect forskolin (FRK)-induced neuritic recruitment. FRK-induced neurites exhibited growth cones and contained secretion granules and many parallel arrays of microtubules as was the case with NGF-induced neurites. FRK, but not NGF, increased the levels of intracellular cAMP and activated adenylate cyclase in the membrane fraction. Both NGF and FRK enhanced the activities of tyrosine hydroxylase (TH), acetylcholinesterase (AchE), and ornithine decarboxylase (ODC), but not the levels of neuron-specific enolase. Enhanced levels of intracellular cAMP mimicked the effects of NGF on neuritic growth, TH, AchE, and ODC activities in PC12D cells, even though NGF does not act through elevation of levels of cAMP.
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PMID:Neuritic growth from a new subline of PC12 pheochromocytoma cells: cyclic AMP mimics the action of nerve growth factor. 303 56

The impact of maternal starvation in late gestation on development of some enzymatic mechanisms concerned with neurotransmission and polyamine synthesis was studied in fetal rat brain. Between 17 and 20 d, acetylcholinesterase and choline acetyltransferase activity increased in fetal brains of fed dams, whereas maternal starvation from day 17 to day 20 resulted in heightened acetylcholinesterase but not choline acetyltransferase activity. Ornithine decarboxylase activity on a per-gram wet-weight basis fell between 17 and 20 d in fetal brain from fed dams. Increasing the duration of maternal starvation resulted in a progressive increase in fetal brain ornithine decarboxylase. Arginine and putrescine levels in the brain were lower in fetuses of starved mothers while spermidine and spermine concentrations were unchanged. Since the Km of ornithine decarboxylase for ornithine was found to vary directly with levels of putrescine in fetal brain, lower concentrations of putrescine and greater ornithine decarboxylase activity in fetal brains from starved mothers suggested that levels of this enzyme may be controlled in part by putrescine. Changes in the maternal nutritional state had no effect on the activity of glutamate decarboxylase in fetal brain, and tissue levels of the product, gamma-aminobutyric acid, were unchanged. Thus changes in ornithine decarboxylase and acetylcholinesterase activity in fetal brain may uniquely reflect biochemical alterations consequent to maternal starvation.
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PMID:Enzyme markers of maternal malnutrition in fetal rat brain. 381 61

Changes in the activity of choline kinase were measured in the cerebellum during development. Early transient increase was found in the enzyme activity just prior to and during birth. This period of increase did not coincide with the periods of transient elevation in ornithine decarboxylase and choline acetyltransferase previously observed in the developing cerebellum. The effects of the naturally occurring polyamines (putrescine, spermidine, and spermine) on choline kinase and choline acetyltransferase activities, and of phosphorylcholine (the product of the reaction catalyzed by choline kinase) on ornithine decarboxylase and choline acetyltransferase activities, were also examined. Choline acetyltransferase activity was not influenced by either polyamines or phosphorylcholine. However, choline kinase activity from 7-day-old, but not from adult, cerebellum was increased 25% in the presence of 4 mM spermine. In contrast, low spermidine concentrations (less than 2 mM) inhibited choline kinase activity selectively in 7-day-old cerebellum. Ornithine decarboxylase activity from 7-day-old cerebellum was inhibited in a concentration-dependent manner by phosphorylcholine. The present data together with other previous reports suggest that: (a) polyamines may play a role in choline utilization during development via their regulation of choline kinase activity, on the one hand, and of acetylcholinesterase activity on the other; and (b) during development, a reciprocal regulation of choline kinase and ornithine decarboxylase activities by their respective reaction products may exist, whereby choline kinase activity is regulated in a complex manner by polyamines and, in turn, ornithine decarboxylase is inhibited by phosphorylcholine.
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PMID:Reciprocal regulation of ornithine decarboxylase and choline kinase activities by their respective reaction products in the developing rat cerebellar cortex. 609 41

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

(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

PC12 cells, a nerve growth factor-responsive clone of rat pheochromocytoma, contain a membrane-bound adenylate cyclase, which can be activated by adenosine analogs. The characteristics of the cyclase response indicate the presence of stimulatory adenosine receptors. Adenosine analogs also produce a marked increase in the ornithine decarboxylase levels of the cells, and the characteristics of this response suggest that it is linked to the adenylate cyclase-stimulatory adenosine receptors. The ornithine decarboxylase response elicited by 5'-N-ethylcarboxamideadenosine (NECA), a potent stimulatory adenosine analog, is synergistic with that produced by nerve growth factor. Differentiation of the cells with nerve growth factor, however, does not substantially alter either the response of cyclase to the adenosine analog or the magnitude of the adenosine-evoked ornithine decarboxylase response. Treatment of the cells with NECA produces an increase in the phosphorylation of a specific non-histone nuclear protein. While causing little or no morphological alteration by itself, NECA is synergistic with nerve growth factor in producing neurite outgrowth in PC12 cells. NECA does not cause an induction of acetylcholinesterase in the cells. NECA does not cause an induction of acetylcholinesterase in the cells, nor does it appear to affect the induction of this enzyme by nerve growth factor.
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PMID:The action of adenosine analogs on PC12 cells. 733 72

In cultured human neuroblastoma cells (SK-N-MC), a plasma membrane-bound besides a lysosomal ganglioside GM3 sialidase was detected. Both activities can be distinguished by the specific activation with detergents, as well as differential inhibition by Cu++. Plasma membrane and lysosomal sialidase specific activities showed strikingly different behaviour during the growth phase of neuroblastoma cells. Thus, the plasma membrane sialidase increased about 15-fold and mirrored cell growth, it differed from the kinetics of ornithine decarboxylase, an early marker of cell proliferation. The lysosomal sialidase, on the other hand, exhibited constant specific activities during growth of the cells, as did lysosomal and plasma membrane marker enzymes. When the sialidase inhibitor 2,3-dehydro-2-deoxy-N-acetylneuraminic acid was included in the culture medium, a profound change in proliferation kinetics was observed, indicating a release from density-dependent control of cell division. Additionally, the inhibitor abolished the increase of the biochemical differentiation marker acetylcholinesterase. The results suggest an important role of the ganglioside sialidase of the plasma membrane in the processes of proliferation control and differentiation in this neuronal cell system.
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PMID:Role of plasma membrane ganglioside sialidase of human neuroblastoma cells in growth control and differentiation. 814 59

Sodium orthovanadate, an inhibitor of protein tyrosine phosphatases, causes increased levels of tyrosine phosphorylation and blocks, at noncytotoxic concentrations, the differentiative response of rat pheochromocytoma (PC12) cells to beta-nerve growth factor (beta NGF) and basic fibroblast growth factor (bFGF) in a reversible manner. It also prevents growth factor-induced neurite proliferation in primed cells and causes the retraction of previously formed neurites, even in the presence of beta NGF or bFGF. It is equally effective in blocking neurite proliferation by 8-Br-cAMP. Zinc chloride and ammonium molybdate, two other inhibitors of tyrosine phosphatases, also cause parallel decreases in neurite proliferation. Orthovanadate generally reduces the transcription of immediate early response genes (TIS 8 and c-fos) and secondary response genes (ornithine decarboxylase (ODC), acetyl-cholinesterase (AChE) and SCG 10) induced by beta NGF, bFGF, EGF, and PMA, albeit in a variable fashion. There was no observed effect on the kinetics of expression as judged by TIS 8 induction by beta NGF and protein kinase C (PKC) downregulation did not change the levels of inhibition by orthovanadate seen in control cells. Orthovanadate does not affect the production of diacylglycerol induced by beta NGF or bFGF. These observations are consistent with the view that growth factor stimulation of differentiation in PC12 cells involves at least one other PKC independent pathway, and that cAMP and PMA (and their active analogs) activate tyrosine kinases (albeit probably secondarily), which are at least partially responsible for their actions. Although the exact site(s) of action of orthovanadate that lead to the inhibition of growth factor-induced neurite proliferation are unknown, the results presented suggest that it prolongs tyrosine phosphorylations by nonreceptor tyrosine kinases that act downstream from the receptor kinases.
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PMID:Effect of nerve growth factor and fibroblast growth factor on PC12 cells: inhibition by orthovanadate. 846 55


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