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:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the presence of ethanol, corticosterone and dexamethasone inhibit choline acetyltransferase and acetyl-cholinesterase activities in cultured fetal brain cells of the rat. These results suggest that corticosteroids may have an important influence on the activity of cholinergic enzymes in the fetal brain may antagonize the effects of ethanol in this setting.
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PMID:Corticosteroid effects on cholinergic enzymes in ethanol-treated fetal brain cell cultures. 318 76

Histochemical analyses demonstrated that the islands of Calleja complex (ICC) in the cat is exceptionally rich in choline acetyltransferase (ChAT) and acetylcholinesterase (AChE). Both enzymes are found in neuropil throughout the complex, as well as in a subset of the satellite neurons accompanying Callejal islands. Lateromedial changes in these cholinergic and cholinesterasic tissue elements were consistent with our previous finding that the feline ICC is cytoarchitecturally divided into five successively more medial types of island-satellite cell ensembles or units. In particular, satellite neurons reactive for ChAT and AChE diminished progressively in size and increased steadily in number from the most lateral to the most medial units. A concomitant increase in neuropil levels of both enzymes suggested that the strong cholinergic innervation of the feline ICC is at least partially derived from satellite cells. This possibility gained further credibility from the additional observation that very fine processes from some ChAT and AChE satellite neurons projected into the terminal-like cholinergic field permeating the granular Callejal islands. The granule cells themselves lacked ChAT and (apart from potentially artifactual cases) AChE, as did adjoining groups of dwarf cells and small pyramidal like neurons. The cholinergic and cholinesterasic satellite neurons were preferentially located above tubercular Callejal islands and in otherwise cell-poor spaces within the isla magna. Such neurons appeared to be isodendritic: they commonly had ovoidal somata with one or two processes lacking enzyme-reactive spines. Depending on the type of ICC unit involved, their mean soma length ranged from 15 to 24 micron, all but the largest of which was distinctly smaller than that of ChAT and AChE cells in striatal or basal nuclear structures. Not all the cholinesterase neurons in the feline ICC are cholinergic, judging from the finding that there are a significantly greater number of satellite neurons containing AChE than ChAT. Three cholinergic features of the feline ICC are especially noteworthy. First, each of the island-satellite cell ensembles in the complex is unified by AChE neuropil often denser than that of adjacent striatal areas. Second, cholinergic neuropil is exceptionally dense in the isla magna and in a subpial band under medial Callejal islands. Third, ChAT neurons in the isla magna are among the smallest cholinergic cells found in the brain.
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PMID:Feline islands of Calleja complex: II. Cholinergic and cholinesterasic features. 319 58

The activities of 2-(alpha-naphthoyl)ethyltrimethylammonium (alpha-NETA) and its beta-isomer (beta-NETA) were studied at various sites of the cholinergic system using isolated enzyme and organ systems. They were selective inhibitors (I50: alpha-NETA, 9 microM; beta-NETA, 76 microM) of choline acetyltransferase (ChA). The inhibition of ChA by both alpha- and beta-NETA was noncompetitive with acetylcoenzyme A or choline as the variable substrate. In these experiments, the inhibitor and both substrates were added simultaneously to the reaction medium, and short reaction times of 10 min were used to determine initial linear velocities. Under these experimental conditions in the presence of substrates, the degree of inhibition of ChA by alpha-NETA was independent of enzyme concentration indicating the reversibility of the inhibition. If ChA was incubated with alpha-NETA for 10 min in the absence of substrates, the degree of inhibition was higher and was not reversible by dialysis of the inhibited ChA. These observations indicate that alpha-NETA is a pseudo-reversible or slowly reversible inhibitor. Neither alpha- nor beta-NETA exhibited significant effects at muscarinic receptors, ganglionic nicotinic receptors, skeletal muscular nicotinic receptors, cholinesterases or carnitine acetyltransferase at concentrations which inhibited ChA. At concentrations higher than their I50 values to inhibit ChA, both antagonized the effects of acetylcholine (ED50: alpha-NETA, 70-80 microM; beta-NETA, 100 microM), histamine and KCl-induced contractions in the guinea pig longitudinal ileal muscle. At high concentrations, alpha-NETA activated acetylcholinesterase (EC50, 360 microM) and inhibited cholinesterase (EC50, 1100 microM).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:2-(alpha-Naphthoyl)ethyltrimethylammonium iodide and its beta-isomer: new selective, stable and fluorescent inhibitors of choline acetyltransferase. 336 52

Acetylcholine and choline acetyltransferase are found in high concentrations in the corneal epithelium of most species, although their function is unknown. We have measured the levels of each in different regions of the rabbit cornea and found that both are much more abundant in central than in peripheral cornea or conjunctival epithelium. Following abrasion of the cornea, epithelial cells from the surrounding cornea or conjunctiva move over rapidly and regenerate. We have assayed choline acetyltransferase and total protein after complete or incomplete abrasion of the corneal epithelium. Acetylcholine-synthesizing activity was not detectable in the regenerating cells until 14-21 days later (depending on the degree of abrasion). Like glycogen and oxidative enzymes, which are also much more abundant in corneal than conjunctival epithelium, choline acetyltransferase regeneration is complete about 28 days after abrasion. In contrast with acetylcholine and choline acetyltransferase, cholinesterase activity is low and its distribution relatively uniform over cornea and conjunctiva. The high ratio of acetylcholine synthesis to cholinesterase activity suggests that acetylcholine released from the corneal epithelium would be able to diffuse to more distant structures within the eye.
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PMID:Regional distribution of acetylcholine and associated enzymes and their regeneration in corneal epithelium. 375 22

Cultures were prepared by dissociating 3-day-old whole chick embryos and plating the dispersed cells on poly-L-lysine-coated dishes in Dulbecco's Modified Eagle's Medium with 10% fetal calf serum. By 48 hr in culture, aggregates and neuritic sprouting were observed. Long neuritic bundles connecting cell aggregates were evident by 4 days in culture. Consistent patterns throughout the lifespan of the cultures were contacts between neurites, and flat isolated cells, presumptively glial, emerged. Throughout the lifespan of the cultures, the cholinergic cell population was characterized histochemically by the method of Karnovsky and Roots and biochemically by assaying choline acetyltransferase. By 4 days in culture, all aggregates showed light cholinesterase-positive staining; however, with days in culture, several aggregates had no staining, and some positive-stained aggregates were interconnected with other aggregates showing only spotted positive staining. Choline acetyltransferase activity showed a developmental profile in agreement with the histological findings. The early presence of choline acetyltransferase activity is taken as indication of the early commitment of cholinergic neurons.
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PMID:Growth patterns of primary cultures dissociated from 3-day-old chick embryos: morphological and biochemical comparisons. 376 86

Cholinergic neurotransmission has been followed in striatum and hippocampus in two inbred strains of mice (C57Bl/6 and Balb/c) during long term alcohol exposure (over a 25 month period) and with aging. Marked strain dependent differences in reactivity of pre- and postsynaptic cholinergic markers to chronic alcohol exposure and aging were demonstrated in both structures. The Balb/c strain exhibits a remarkable long lasting tolerance to alcohol injury for striatal and hippocampal cholinergic markers (choline acetyltransferase, high affinity choline uptake, muscarinic receptors affinity, acetyl cholinesterase), whereas C57Bl mice appear more sensitive to alcohol intoxication. Likewise aging affects the C57Bl mouse more severely than the Balb/c, a phenomenon which may be involved in the sensitivity of these mice to alcohol intoxication. Moreover long term alcohol exposure, in addition to aging show unequal effects on the diverse cholinergic markers studied. Also divergences of specific brain areas have been noted and should be related to their particular neuroanatomy. Such discrepancies may, in part, explain differences observed in the behavioral effects of chronic alcohol intoxication in alcoholics.
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PMID:Influence of mouse genotype on responses of central cholinergic neurotransmission to long term alcohol intoxication. 377 44

The molecular forms of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) were studied in frontal cortex (grey and white matter), postmortem, and in cerebrospinal fluid (CSF) of demented patients with Parkinson's disease compared to controls and non-demented parkinsonians. In the frontal cortex, AChE activity decreased significantly in both demented and non-demented parkinsonian subjects compared to controls; the 10S form of the enzyme was significantly lower in demented parkinsonians than in the non-demented subjects. The decrease in AChE activity was correlated with a decrease in choline acetyltransferase activity thought to reflect lesion of cholinergic neurones in the substantia innominata which innervate the cerebral cortex. BChE activity decreased only in the non-demented parkinsonians; in the demented subjects, BChE activity was at control levels. Similar results were obtained with grey and white matter, although absolute levels of the two enzymes were different in the two types of tissue, suggesting that the enzymes were affected in the cholinergic neurones before transport to cortical nerve terminals. No decreases in AChE or BChE activity were observed in the CSF of the patients studied. On the contrary, AChE and BChE levels were significantly higher in demented parkinsonian patients compared to the non-demented subjects.
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PMID:Acetylcholinesterase and butyrylcholinesterase in frontal cortex and cerebrospinal fluid of demented and non-demented patients with Parkinson's disease. 394 70

N1E-115 neuroblastoma cells were grown in the absence or presence of atropine (1 microM) for 9 days. After 9 days membranes were prepared from control and atropine-treated cells. They were stored frozen until some markers of muscarinic cholinergic function were measured. Atropine treatment increased the number of muscarinic receptors from 100 +/- 10 fmol/mg protein to 145 +/- 20 fmol/mg protein, decreased the cholinesterase activity from 3.5 +/- 2.0 U/mg protein to 1.0 +/- 0.5 U/mg protein and increased the choline acetyltransferase activity from 0.25 +/- 0.13 pmol [3H]acetylcholine synthesized/min X mg protein to 1.80 +/- 0.59 pmol [3H]acetylcholine synthesized/min X mg protein. It is suggested that all these changes are correlates of muscarinic receptor supersensitivity.
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PMID:Long time treatment of N1E-115 neuroblastoma cells with atropine induces changes in markers of muscarinic cholinergic function. 396 Mar 99

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

Converging lines of evidence indicate an important role for the basal forebrain cholinergic system in memory processes. The principal origin of the cholinergic projection to the neocortex appears to be the magnocellular neurons in the region of the nucleus basalis of Meynert (NbM). We examined the effects of bilateral lesions of the NbM on retention of shock avoidance training by stereotaxically injecting rats with 0.5 microliter of ibotenic acid (14 micrograms/microliter) into the NbM. Two weeks later rats were given passive avoidance training and tested for retention of the original avoidance habit 5 min, 30 min, or 24 hr later. Rats with lesions of the NbM showed significantly impaired shock avoidance performance compared to non-operated controls at both 30 min and 24 hr, but not at 5 min after training. Lesioned animals also showed a significant decrease in cortical choline acetyltransferase (CAT) and acetylcholinesterase (AChE) activities. No differences in muscarinic receptor binding or plasma cholinesterase activity was observed. The results demonstrate the usefulness of NbM lesions as a model for studying the role of the basal forebrain cholinergic system in memory processes.
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PMID:Further characterizations of the nature of the behavioral and neurochemical effects of lesions to the nucleus basalis of Meynert in the rat. 402 31


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