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 effects of epidermal growth factor on high density primary cultures of fetal (embryonic day 17) rat septal cells were examined. Under serum-free conditions, the continuous exposure of these cultures to epidermal growth factor for seven days significantly decreased choline acetyltransferase (EC 2.3.1.6) activity in a dose-dependent manner. Maximal decreases were observed from 1 to 10 ng/ml epidermal growth factor. This effect was completely abolished by the addition of anti-epidermal growth factor antibodies. The epidermal growth factor-mediated decrease in choline acetyltransferase activity was culture-time dependent, being first detectable after five days of factor application and may likely represent an inhibition of the spontaneous increase in enzyme activity that occurs with time in culture. Concomitant with changes in enzyme activity, epidermal growth factor produced a significant and proportional decrease in the number of acetylcholinesterase-positive neurons. This decrease in acetylcholinesterase-positive cells did not reflect a decrease in cholinergic cell survival as nerve growth factor could restore the number of acetylcholinesterase-positive neurons in epidermal growth factor-treated cultures to control levels. Furthermore, in these high-density cultures, epidermal growth factor did not affect general neuronal survival, while it did produce an increase in the number and intensity of glial fibrillary acidic protein-immunoreactive astroglia as well as in the number of macrophage-like cells. The proliferative response of these non-neuronal cells to epidermal growth factor, as assessed by [3H]thymidine incorporation, was evident after three days of epidermal growth factor application, persisted thereafter, and could be antagonized by the inclusion of the antimitotic 5-fluorodeoxyuridine. Furthermore, 5-fluorodeoxyuridine completely blocked the epidermal growth factor-mediated decrease in choline acetyltransferase activity. However, when epidermal growth factor was tested in pure glial cultures, it only directly induced proliferation of astrocytes. These results suggest that the proliferative response of either one or both of these glial cell types in the mixed cultures may be indirectly affecting cholinergic cell expression.
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PMID:Epidermal growth factor affects both glia and cholinergic neurons in septal cell cultures. 140 62

A primary culture system of nearly pure neuronal cells from 14-day-old fetal rat spinal cord has been developed by combining a preplating step, the use of a chemically defined serum-free medium, and borated polylysine-coated dishes that prevented the formation of cell aggregates. About 98% of the cells were found to be immunostained with neuron-specific enolase antibodies, confirming their neuronal nature. The cultures are composed essentially of a population of non-motoneurons and contain few motoneurons, characterized by their large size and multipolar aspect, the presence of acetylcholinesterase (AChE), and the intense immunoreaction for growth-associated protein GAP-43. Neuronal precursor cells are also present in these cultures and proliferate during the first 3 days. The addition of bovine brain basic fibroblast growth factor (bFGF) stimulates their proliferation over a period of 2 days, as determined by measurement of [125I]iododeoxyuridine incorporation and by immunocytochemical reaction after bromodeoxyuridine incorporation into nuclei. The proliferating cells were characterized as neurons by immunostaining against neuron-specific enolase. Recombinant human bFGF and bovine brain acidic FGF (aFGF) exerted similar effects. Other growth factors, including epidermal growth factor (EGF), transforming growth factor beta 1 (TGF-beta 1), and thrombin, were without effect on the proliferative activity of these neuronal cells. bFGF has no effect on the survival of motoneurons and on the fiber outgrowth of the whole neuronal population. However, bFGF affects the development of bipolar AChE-positive neurons, probably belonging to the non-motoneuron population. The data indicate that bFGF and aFGF are mitogens for neuroblasts from rat spinal cord in culture and that bFGF influences the development of a subpopulation of spinal neurons that are AChE-positive.
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PMID:Establishment of pure neuronal cultures from fetal rat spinal cord and proliferation of the neuronal precursor cells in the presence of fibroblast growth factor. 172 69

A new method has been described for removing a very small number of contaminating astrocytes in neuronal cultures (derived from the septal-diagonal band region of 17-day-old embryonic rat brain) grown in a chemically defined medium. The proportion of these glial fibrillary acidic protein (GFAP)-positive cells was usually less than 1.5% up to 10 days, but thereafter their number increased rapidly reaching 10-15% by 22 days in vitro. A prolonged exposure to normally used concentration of cytosine arabinoside (Ara-C; 10 microM) was toxic to both astroglial and neuronal cells, while a brief treatment (48 h) with a low level (4 microM) of Ara-C failed to eliminate these astrocytes, as judged by glutamine synthetase activity and GFAP-positive cell count. However, these quiescent astroglial cells could be easily eliminated if they were induced to proliferate by epidermal growth factor before exposure to Ara-C. The combined treatment with these agents had no effect on the number of acetylcholinesterase-positive cells, and on the development of cholinergic and GABA-ergic neurons, as measured in terms of choline acetyltransferase and glutamate decarboxylase activity, respectively.
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PMID:A novel way of removing quiescent astrocytes in a culture of subcortical neurons grown in a chemically defined medium. 290 25

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

Neurons dissociated from the septal area of fetal rat brains were grown in culture. Cholinergic neurons were identified by immunocytochemical visualization of choline acetyltransferase and cytochemical demonstration of acetyl cholinesterase. Choline acetyltransferase immunocytochemistry stained cell bodies and proximal processes while acetylcholinesterase cytochemistry visualized the entire neuron. Choline acetyltransferase-positive neurons could only be identified in cultures grown under conditions that produced the maximal choline acetyltransferase activity, measured biochemically. All of the choline acetyltransferase-positive neurons were double stained for acetylcholinesterase while only 6% of the acetylcholinesterase-positive cells were choline acetyltransferase negative in these cultures. These results indicate that acetylcholinesterase is a reliable marker for cholinergic cells in cultures of dissociated septal neurons. Being the more sensitive method, acetylcholinesterase staining was therefore used to identify cholinergic cells in cultures with choline acetyltransferase levels insufficient for immunocytochemical visualization of this enzyme. Addition of nerve growth factor or antibodies to nerve growth factor to the medium did not affect the number of cholinergic neurons surviving in culture. Furthermore, nerve growth factor and anti-nerve growth factor failed to influence the general morphological appearance and the number of processes of these neurons. However, nerve growth factor elevated the biochemically measured activity of choline acetyltransferase up to two-fold. The nerve growth factor-mediated increase in choline acetyltransferase activity was dose dependent with an ED50 of 10 ng/ml (4 X 10(-10) M). The increase was highly specific for nerve growth factor. It was blocked by anti-nerve growth factor, and epidermal growth factor, insulin and other control proteins failed to exert a similar effect. Nerve growth factor had to be present for at least 3 days in the culture medium to increase choline acetyltransferase activity, suggesting that the increase was due to an elevated choline acetyltransferase synthesis rather than to an activation of the enzyme.
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PMID:Nerve growth factor increases choline acetyltransferase but not survival or fiber outgrowth of cultured fetal septal cholinergic neurons. 397 85

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

Exposure of naive PC12 cells, sympathetic neurons from rat superior cervical ganglia, and brain-derived septal neurons to epidermal and nerve growth factors simultaneously resulted in some alteration of cellular events induced by nerve growth factor alone. A more pronounced decline of catecholamine content, no additional change in acetylcholinesterase activity, and additive stimulation of RNA and protein syntheses were found in PC12 cells. Earlier elevation of the enzyme activity was observed in sympathetic but not in septal neurons. Epidermal growth factor appeared to support independently the same level of acetylcholinesterase activity in septal neurons as revealed for nerve growth factor during the first week and cell survival throughout 2 weeks of observation. The data obtained indicate that epidermal growth factor augments temporarily some effects of nerve growth factor, thus supporting the idea of an important role of mitogenic growth factors in neural development as complementary and/or substitutive regulators of nerve cell differentiation and survival.
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PMID:Epidermal growth factor influences the neurotrophic/differentiating action of nerve growth factor. 748 19

Numerous studies suggest that growth and trophic factors play roles in the development and mature function of brain neurons. Recently, growth factors whose actions were previously characterized on non-neuronal cells have been localized to the brain. We sought to determine whether these factors influence septal cholinergic function. Initially, we defined the effects of basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) on septal cholinergic cells in dissociated neuronal culture. Both factors elevated activity of the acetylcholine synthetic enzyme, choline acetyltransferase (CAT). To determine whether the factors acted directly on neurons or whether glia mediated the effects, a mitotic inhibitor, 5-fluorodeoxyuridine (FDUR), was added to the cultures to eliminate dividing glia. The action of EGF was completely blocked by the addition of FDUR. However, bFGF elevated CAT activity even in the presence of FDUR. Consequently, bFGF may regulate septal cholinergic function directly, whereas EGF may affect cholinergic cells indirectly through glia. To determine whether increases in CAT activity reflect increased enzyme activity per neuron or an increase in the number of cholinergic cells, bFGF-treated cultures were stained for acetylcholinesterase (AChE) to determine numbers of cholinergic cells. No differences in AChE-positive cells were noted, suggesting that bFGF increased CAT activity per cholinergic neuron. To determine whether bFGF regulates other populations in the septum, we examined GABAergic neurons by monitoring the activity of glutamic acid decarboxylase (GAD), a GABA synthetic enzyme. Basic FGF significantly increased GAD activity; however, the effect was completely abolished by addition of FDUR. Thus, bFGF may act directly on cholinergic neurons and indirectly on GABA cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Septal neuron cholinergic and GABAergic functions: differential regulation by basic fibroblast growth factor and epidermal growth factor. 802 75

Unlike nerve growth factor (NGF), epidermal growth factor (EGF) does not induce neuronal differentiation but promotes proliferation of the rat pheochromocytoma PC12 cells. We found that PC12h-R, a subclone of PC12 cells, differentiated into neuron-like cells in response to EGF as well as to NGF. PC12h-R cells treated with EGF extended neurites, attenuated cell proliferation, and increased the levels of tyrosine hydroxylase protein synthesis and of acetylcholinesterase activity as those treated with NGF. The EGF-induced differentiation of PC12h-R cells was not mediated by the indirect activation of p140trkA by EGF. In addition, EGF induced the sustained tyrosine phosphorylation of the EGF receptor, mitogen-activated protein (MAP) kinases, and 46 and 52 kDa proteins, and the prolonged activation of MAP kinases in PC12h-R cells compared with the parent PC12h, which does not show EGF-induced differentiation. The response of PC12h-R cells to EGF was not simply due to an increase in the level of EGF receptor protein. These results indicated that the duration of EGF-induced signaling might determine the cellular response of PC12 cells between cell proliferation and neuronal differentiation.
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PMID:PC12h-R cell, a subclone of PC12 cells, shows EGF-induced neuronal differentiation and sustained signaling. 871 24

The effects of transforming growth factor alpha (TGF alpha) on low and high density cultures of fetal (embryonic day 17) rat medial septal cells were investigated and in some instances, compared to those of epidermal growth factor (EGF). In high density cultures, TGF alpha induces a significant increase in the number of astroglia and microglia. While the effects of TGF alpha on the astroglia are more pronounced when compared to EGF, those on the microglia are less notable. In addition, TGF alpha produces a time- and dose-dependent decrease in the activity of choline acetyltransferase (EC 2.3.1.6) and a proportional decrease in the number of acetylcholinesterase-positive neurons in these high density cultures. However, although both EGF and TGF alpha decreased choline acetyltransferase activity maximally at the same concentration (10 ng/ml), the latter was consistently more potent. TGF alpha does not affect cholinergic cell survival but the expression of their chemical phenotype and does so indirectly via the glial cells. On the other hand, TGF alpha directly induces a dose- and time-dependent increase in glutamic acid decarboxylase activity in these high density cultures without affecting the number of glutamic acid decarboxylase immunoreactive neurons. In low density cultures, TGF alpha acts as a general neuronal survival factor, affecting both cholinergic and GABAergic neurons. Here TGF alpha's neurotrophic activity is more evident than its effects on their chemical phenotype. These results suggest that TGF alpha exerts distinct and differential effects on the biochemical expression of two neuronal populations in the developing medial septum maintained in high density culture. Finally, as TGF alpha acts as a general neuronal survival factor in low density cultures, cell to cell interactions appear to be important in the ultimate response of these cells to this growth factor.
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PMID:Transforming growth factor alpha differentially affects GABAergic and cholinergic neurons in rat medial septal cell cultures. 886 17


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