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)

C57BL/6J mice, age 6-8 weeks were inoculated intracerebrally with brain homogenate from mice previously infected with the 139A strain of scrapie; control mice were identically treated with brain homogenate from non-infected normal mice. The activities of choline acetyltransferase (CAT), acetyl cholinesterase (AChE), and glutamic acid decarboxylase (GAD) were determined in the forebrain and hindbrain of these animals after 67, 126 and 151 days post-inoculation. There were no significant differences in the activities of CAT and GAD between scrapie and control mice at early, middle or late stages of the disease in the scrapie-infected animals; there was an about 20% decline in AChE activity in the scrapie brain.
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PMID:Brain glutamate decarboxylase and cholinergic enzyme activities in scrapie. 403 59

Conditions have been developed for the culture of rat spinal cord neurons in serum-free media supplemented with hormones and growth factors. Neurons were identified by immunofluorescence-labeled anti-neurofilament antibody, and their growth was monitored by assay of choline acetyltransferase and cholinesterase activities. Activities of these enzymes were considerably higher than those of comparable cultures in serum supplemented media in which there were visibly many more nonneuronal cells. Serum immunoglobulins from patients with motor neuron disease showed enhanced binding to rat spinal cord cells maintained in both serum-supplemented and serum-free media, as compared with those from normal healthy individuals. Enhanced binding was more marked with the latter cells, presumably because of the higher proportion of neuronal cells in these cultures. Serum immunoglobulins from patients with other neurologic disorders showed a similar binding to that of the normal controls. The results demonstrate the presence of an immune response to spinal cord cell membrane components in patients with motor neuron disease, although whether the response is primary or secondary in the disease process remains unclear.
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PMID:Cultured rat spinal cord neurons: interaction with motor neuron disease immunoglobulins. 404 91

Effects of nine choline ethers, (CH3)3 NCH2CH(R)-O-R', on the muscarinic and nicotinic receptors of longitudinal smooth muscle of guinea-pig ileum were studied to understand the role of electronic/steric factors at the ether-oxygen in stimulating the cholinergic receptors. Their ED50S to cause contraction of the ileum in presence of hexamethonium (37 X 10(-6) M) were 2 to 307 times higher than that of acetylcholine (ACh; 2.9 X 10(-7) M). The relative maximal effects of 5 ethers (1.20 to 1.34) were higher than that of ACh (1.0), while 4 exhibited lower maximal effects (less than 0.71). These ethers exhibited no significant inhibition of choline acetyltransferase and cholinesterase activities from the longitudinal muscle at their ED50S. Hexamethonium significantly increased the ED50S of 5 choline ethers. The ED50S of some of the ethers also were significantly increased by treating the muscle with physostigmine (38.5 X 10(-8) M) or physostigmine and hexamethonium. Atropine (greater than 1 X 10(-6) M) blocked the contractions induced by these ethers. The steric hinderance caused by the beta-methyl and/or O-alkyl groups and the electron density around the ether-oxygen are limiting the muscarinic, as well as nicotinic, potencies of these choline ethers. Choline ethers possessing the beta-methyl and O-n-propyl, iso-propyl or ter-butyl groups presumably release ACh at a site causing inhibitory potential through a secondary pathway.
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PMID:Cholinergic properties of choline ethers. 406 29

Recent studies have renewed interest in the role of acetylcholine (ACh) in the cognitive changes associated with ageing and dementia. Deficits in cortical choline acetyltransferase (ChAT) in Alzheimer's disease have been consistently demonstrated, while other research has suggested a connection between deterioration of cortical ACh fibres and dementia. However, despite clear biochemical and anatomical evidence for a fall in ACh in dementia, results of therapeutic trials with cholinergic agonists, precursors and cholinesterase inhibitors have been inconsistent. Such findings suggest that cortical cholinergic disorders are not wholly a function of simple biochemical change; alterations of impulse flow along cholinergic fibres could well be as debilitating. An important extrinsic source of cortical ACh innervation derives from neurones diffusely located in rat basal forebrain, denoted the nucleus basalis (NB). We have now investigated the impulse conduction properties of cortically projecting, putatively cholinergic NB axons in adult and aged rats and have found that conduction latencies from NB to frontal cortex are significantly longer (by 51%) in aged animals. In addition, systematic analysis varying cortical stimulation depth revealed that these longer latencies are due entirely to decreased conduction velocities in the subcortical fibre projections. Indeed, intracortical velocities were virtually identical in the two groups. Our results indicate that ageing occasions a decrease in the temporal fidelity of impulse flow in the cholinergic input to the cortex from the NB, a previously overlooked but potentially important element in cognitive deficits that occur with age.
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PMID:Age-impaired impulse flow from nucleus basalis to cortex. 406 17

Redistribution of axonal enzymes as a function of time in vitro was studied in an unbranched segment of frog sciatic nerve. Cholinesterase activity moved peripherally at a rate of 99 mm/day and centrally at 19 mm/day. One-quarter of the total nerve content of the enzyme was estimated to be in motion, one-eighth in each direction. Mitochondrial enzymes (hexokinase and glutamic dehydrogenase) moved peripherally at 20-31 mm/day, centrally at 11-20 mm/day. Only 10% of the total content of these mitochondrial enzymes was in motion. No movement of choline acetylase or 6-phosphogluconic dehydrogenase activity was seen even after 4 days in vitro. However, in a 12 day in vivo experiment choline acetylase moved toward the periphery at a rate of 0.34 mm/day. After a day or so in vitro the distal accumulations of cholinesterase and glutamic dehydrogenase decreased, with a concomitant and quantitatively equivalent increase in enzyme activities at the proximal end of the nerve. It is postulated that during incubation a mechanism for reversing the direction of flow develops in the peripheral stump of the nerve. Vinblastine inhibited central and peripheral flow of both cholinesterase and glutamic dehydrogenase. Movement of cholinesterase was not affected by ouabain, thalidomide, or phenobarbital, nor by K(+) excess (110 mM) or absence.
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PMID:Transport of axonal enzymes in surviving segments of frog sciatic nerve. 411 99

1. Acetylcholine (ACh), cholinesterases and choline acetyltransferase (choline acetylase) were estimated in the neural lobe and hypothalamus of the adult male rabbit. Acetylcholine was also estimated in the neural lobes and hypothalami of some other mammals.2. Acetylcholine-like activity was measured by bio-assay using the leech dorsal muscle preparation.3. Characterization experiments indicated that about 90% of the activity measured was due to acetylcholine.4. Mean acetylcholine content in the neural lobe of the rabbit, after extraction with perchloric acid, was 4.38 +/- 0.98 mug/g fresh tissue, and 4.87 +/- 1.53 mug/g in the hypothalamus.5. Acetylcholine was also found to be present, in comparable concentrations, in the neural lobe of man and in the neural lobes and hypothalami of ox, rat and hedgehog.6. Acetylcholinesterase, present in the neural lobe and hypothalamus of the rabbit, hydrolysed 1.74 +/- 0.11 mu-moles of substrate/min/g and 3.78 +/- 0.60 mu-moles substrate/min/g fresh tissue respectively.7. The concentration of butyrylcholinesterase was about one tenth that of acetylcholinesterase in both tissues.8. Choline acetyltransferase present in the neural lobe and in the hypothalamus synthesized 87 +/- 22 mug ACh/hr/g fresh tissue and 378 +/- 149 mug respectively.
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PMID:Acetylcholine and related enzymes in the neural lobe and anterior hypothalamus of the rabbit. 430 97

Overt neurological impairment is the endpoint currently used to document a case of methylmercury poisoning. No consideration is given to possible subtle consequences. Offspring from mice exposed to methylmercury on day 7 or 9 of pregnancy were apparently unaffected during postnatal development. However, subtle behavioral differences between treated and control offspring were found when the overtly normal animals were tested in an open field and evaluated in a swimming apparatus at 1 month of age. Brain weight, protein, choline acetyltransferase, and cholinesterase were not significantly altered.
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PMID:Subtle consequences of methylmercury exposure: behavioral deviations in offspring of treated mothers. 504 6

Several markers of chick neuroretinal differentiation were monitored in vivo and in culture. All increase markedly between 7 and 20 days of embryonic development in vivo. In vitro, endogenous GABA levels decrease almost immediately, while other neuronal markers increase as in vivo for 2 to 5 days before declining (choline acetyltransferase, acetyl cholinesterase, glutamic acid decarboxylase). Neuronal cell surface markers (binding sites for tetanus toxin, alpha-bungarotoxin, muscimol), however, reach maximal levels only after 8 days in vitro. Glial markers such as carbonic anhydrase and hydrocortisone-induced glutamine synthetase activities are also expressed only transiently in culture.
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PMID:Expression of differentiation markers by chick embryo neuroretinal cells in vivo and in culture. 614 Feb 94

The intralaminar distributions of transmitter and nontransmitter enzyme activities and amino acid levels were determined in the midtemporal cortices from normal individuals and established cases of Alzheimer's disease. In the normal, choline acetyltransferase (CAT) and acetylcholinesterase (AChE) activities were relatively high in the outer cortical layers, particularly, for CAT, in the two granular layers (II and IV). Both activities were reduced in Alzheimer's disease at all, although generally most extensively in the outer and middle layers of the grey matter whereas activities were near normal in the white matter. Further, the enzyme distribution patterns of these cholinergic activities were also disrupted in Alzheimer's disease and the activity of CAT throughout the cortex was generally reduced to that found in the white matter. No such differences in distribution were found for two other enzymes, pseudocholinesterase and lactate dehydrogenase. Assessment of the gamma-aminobutyric acid (GABA) system in the normal revealed a much more extensive intralaminar variation in the enzyme, glutamate decarboxylase, compared with the level of GABA itself. In contrast with the cholinergic enzymes, neither the levels nor intralaminar patterns of GABA were altered in Alzheimer's disease. From an analysis of free amino acids at the different cortical levels, the cortical pattern of glutamic acid in the normal was different from that for GABA, aspartic acid, or nontransmitter amino acids such as alanine. Neither of the putative amino acids, glutamate or aspartate, was altered in Alzheimer's disease. These findings demonstrate the relatively selective nature of microchemical changes occurring in the cortex in Alzheimer's disease and suggest that a functional abnormality in cholinergic input to the outer neocortical layers (I-IV) with predominantly receptive and associative functions may be an important feature of the disease.
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PMID:Intralaminar neurochemical distributions in human midtemporal cortex: comparison between Alzheimer's disease and the normal. 614 24

Two cyclic choline analogues (3-hydroxy-N,N- dimethylpiperidinium and 2-hydroxymethyl-N,N- dimethylpiperidinium ) and two cyclic homocholine analogues (4-hydroxy-N,N- dimethylpiperidinium and 3-hydroxymethyl-N,N- dimethylpiperidinium ) have been studied with regard to their actions at the cholinergic synapse. All the analogues had some direct depolarizing activity on the frog rectus abdominis muscle but they were less potent in this respect than acetylcholine. Compared to physostigmine, the analogues were weak inhibitors of cholinesterase enzymes. All the analogues were found to have a presynaptic blocking action on the rat phrenic nerve-hemidiaphragm preparation, which was reversed by choline. In addition, they all inhibited the high affinity transport of choline into synaptosomes but only the cyclic choline analogues were found to be acetylated by soluble choline acetyltransferase in vitro. We conclude that the hydroxypiperidinium analogues caused the presynaptic block seen at the neuromuscular junction by inhibiting acetylcholine synthesis.
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PMID:Pharmacological actions of some cyclic analogues of choline. 632 23


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