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)

Electrophysiological, microiontophoretic and neuroanatomical techniques have been employed to investigate the relationships between intrastriatal sites of dopamine/glutamate (DA/GLU) interaction and inhomogeneities for acetylcholinesterase. The sites where iontophoretically applied DA antagonized the excitatory effects of iontophoretic GLU or cortical stimulation showed no topographic arrangement in the dorsolateral parts of the striatum. The data suggest that DA/GLU interaction in the striatum of the adult rat may occur independently from distribution of acetylcholinesterase.
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PMID:[Dopamine-glutamate interaction and cholinesterase activity in the corpus striatum of the adult rat]. 262 49

Nonsynaptic mitochondria isolated from rat brain hippocampus were compared with those obtained by means of the same preparative procedure from cerebral cortex and striatum. Protein recovery, marker enzyme activities (lactate dehydrogenase, citrate synthase, and acid phosphatase), state 4 respiration, and response to hypoosmotic shock showed no difference among the three cerebral regions, suggesting homogeneous behavior during the subfractionation procedure. Cholinergic markers--choline acetyltransferase, acetylcholinesterase activities, and high-affinity choline uptake--evaluated on synaptosomes showed the classic regional pattern with an enrichment in the striatum (striatum much greater than hippocampus). The coupling state of the mitochondrial fractions was maintained (respiratory control ratios ranging from 3.62 to 5.08 with glutamate + malate as oxidizable substrates), showing a metabolic competence sufficient to perform metabolic studies. Regional differences were found in state 3, uncoupled state of respiration, and cytochrome oxidase activity. Hippocampus showed the lower values (hippocampus less than striatum less than cortex). A possible role of this lower capacity of mitochondrial energy metabolism in determining the sensitivity of hippocampal neurons to ischemia or epileptic seizures is suggested.
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PMID:Oxidative metabolism of nonsynaptic mitochondria isolated from rat brain hippocampus: a comparative regional study. 283 1

Bath application of glutamate at two concentration ranges, 10(-6)-10(-8) and 1-3 X 10(-3) M, effectively increased acetylcholinesterase activity in cerebellar slices obtained from 8-day-old rats. No such effect was seen in cerebellar slices of 7-week-old rats or cerebral slices of either 7-week or 8-day-old rats. Glutamic acid diethyl ester blocked the glutamate effect at both of these concentration ranges, suggesting that quisqualate-sensitive glutamate receptors are involved in regulation of acetylcholinesterase activity in early postnatal cerebellum. Since bath application of cyclic GMP at 10(-7)-10(-9) M increased the acetylcholinesterase activity in cerebellar slices of 8-day-old rats, it is possible that glutamate-dependent regulation of acetylcholinesterase activity is mediated by cyclic GMP. The observation that adenosine deaminase blocked the effect of glutamate completely at 10(-6)-10(-8) M and partially at 1-5 X 10(-3) M further suggests that release of adenosine is a link from enhanced cyclic GMP activity to activation of acetylcholinesterase.
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PMID:Glutamate-elicited stimulation of acetylcholinesterase activity in cerebellar slices from newborn rats. 287 25

Male rats were treated bi-weekly by gavage with the equivalent of 0.5 mg X kg-1 X day-1 technical diazinon for up to 28 weeks. The animals were sacrificed at specific time intervals (7, 14 and 28 weeks) and compared with age matched controls. Blood and brain tissues were analysed for cholinesterase activity and for concentrations of catecholamines and amino acids. Only Plasma cholinesterase was significantly reduced by the low level pesticide treatment. Erythrocyte acetyl cholinesterase and brain acetyl cholinesterase were unchanged while during the same period several putative brain neurotransmitters aspartate, glutamate (excitatory) and taurine as well as GABA (inhibitory) were significantly reduced in experimental vs control animals whereas no significant changes occurred between weeks in similarly fed animals. Blood serotonin was significantly elevated but no other blood or brain monoamine was significantly altered. Overt manifestations of brain toxicity observed were not apparent in experimental compared with control animals save for a significant decrease in growth observed in experimental animals. It was concluded that oral administration of low doses of diazinon exerts significant effects other than as an anticholinesterase on important brain neurotransmitters even at the low dose levels administered in this study.
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PMID:Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. 287 63

The potassium-stimulated release of acetylcholine (ACh), glutamate (GLU) and dopamine (DA) from mouse striatal slices was studied during anoxia and/or 3,4-diaminopyridine (DAP) treatment. Anoxia, in the presence of calcium, increased DA and GLU release, but depressed ACh release. Omission of calcium from an anoxic incubation further stimulated GLU and DA release and impaired ACh release. Under normoxic conditions, DAP (100 microM) increased the release of all three neurotransmitters; the sensitivity of the slices to DAP changed with the presence or absence of an acetylcholinesterase inhibitor in the preincubation media. During an anoxic incubation, DAP did not ameliorate the anoxic-induced, K+-stimulated impairment of ACh release, but significantly reduced the K+-stimulated release of GLU and DA. These results are consistent with the hypothesis that hypoxia induces a presynaptic deficit that may underlie postsynaptic ischemic-induced changes. Amelioration of these presynaptic alterations in neurotransmitter release may be an effective approach to preventing hypoxic-induced damage.
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PMID:Differential alteration of dopamine, acetylcholine, and glutamate release during anoxia and/or 3,4-diaminopyridine treatment. 289 Oct 59

Addition of the acetylcholinesterase inhibitor 1,2,3,4-tetra-9-hydroaminoacridine (THA) at 1-3 mM markedly reduced the neuronal cell loss that otherwise followed brief exposure of murine cortical cell cultures to 500 microM N-methyl-D-aspartate (NMDA). This novel antagonism was selective for NMDA receptor-mediated toxicity, as it extended to glutamate toxicity but not to quisqualate toxicity, and was THA concentration-dependent between 100 microM and 3 mM, with IC50 approximately 500 microM. The antagonism was probably not due to enhancement of endogenous cholinergic action, as it was not mimicked by acetylcholine, carbachol, or bethanechol; rather, it likely reflected a recently described interaction of THA with the phencyclidine receptor. Exploration of structural specificity revealed some partial neuron-protection with high concentrations of other cholinesterase inhibitors--physostigmine, neostigmine, and edrophonium, but not the structurally related potassium channel blocker, 4-aminopyridine. Further examination of correlations between THA-like structure, and neuron-protective activity, may provide useful insights in the development of new antagonists of NMDA receptor-mediated neurotoxicity.
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PMID:Tetrahydroaminoacridine selectively attenuates NMDA receptor-mediated neurotoxicity. 290 64

A three-dimensional reconstruction of high endothelial venules (HE-venules) of an entire mouse lymph node is presented. The reconstruction has been made by means of the histochemical technique for alpha-naphthylacetate esterase. The course of the HE-venules is shown in coherence with lymphocytic aggregates (follicles and unit), which were concomitantly reconstructed. Carbonic anhydrase, glutamate-, and alpha-glycerophosphate dehydrogenase were found in the high endothelia, while calcium-stimulated NA+, K+ ATP-ase and the acetylcholinesterase were localized to the endothelia and/or to the perivascular sheath of the HE-venules and submarginal capillaries.
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PMID:A three-dimensional reconstruction of high endothelial venules in the mouse lymph node: an enzyme-histochemical study. 293 5

Dopamine D2 receptors, labeled with [3H]spiroperidol or [3H]sulpiride, show a lateral-to-medial gradient in the caudate-putamen, with a more than two-fold greater density laterally than medially. It has been thought that D2 receptors are located on at least two neuronal elements of the caudate-putamen, neurons intrinsic to this structure and axons whose cell bodies reside in the cortex. As a first step in establishing what neuronal elements underlie this heterogeneous organization of D2 receptors, we took advantage of quantitative autoradiography to examine the association of these receptors with those elements. The present findings show that the D2 sites are almost exclusively located on neurons whose somata reside in the caudate-putamen and are not located on terminals of corticostriatal axons. A detailed comparison of the distribution of histochemically identified acetylcholinesterase neurons with that of D2 receptors in serially adjoining sections suggests a common organizational pattern. The density of [3H]spiroperidol sites in rat caudate-putamen was determined after unilateral injection of the neurotoxin quinolinic acid into this structure or after ablation of neocortical regions. Quantification of the tissue damage was achieved by acetylcholinesterase histochemistry (following diisopropylfluorophosphate treatment), as well as by thionin and luxol fast staining of sections adjacent to those used for [3H]spiroperidol autoradiography. In identically treated animals, biochemical determination of the extent of tissue damage was made utilizing assays for high-affinity [3H]choline and [3H]glutamate uptake in the caudate-putamen. In quinolinic acid-injected rats, the density of D2 sites was decreased by 90-95% at the site of complete loss of large acetylcholinesterase-positive neurons. Other animals, given ablations of specific neocortical fields (medial prefrontal, motor, somatosensory) or of the entire parietal-frontal cortex of one hemisphere, showed no loss of caudate-putamen D2 sites unless the cortical ablation caused accompanying damage of the caudate-putamen. In the caudate-putamen of all animals there was a close correspondence between the D2 sites and the striatal neurons (and processes) that show strong acetylcholinesterase reactivity. We suggest that the caudate-putamen topography of D2 sites is based largely on the internal organization of this structure and may preferentially involve acetylcholine-containing intrinsic neurons.
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PMID:Quantitative autoradiography of dopamine D2 sites in rat caudate-putamen: localization to intrinsic neurons and not to neocortical afferents. 295 47

Growing rats were fed ad libitum soy protein isolate (SPI) or its peptic (SPI-P) or tryptic digest (SPI-T) for a month and their sera were examined for cholesterol and triglyceride levels and enzyme activities such as cholinesterase, glutamate-pyruvate transaminase (GPT) and alkaline phosphatase. The rats fed SPI-P or SPI-T were inferior in growth to those fed SPI. Similarly, the serum glyceride level was lower in the SPI-P and SPI-T groups than in the SPI group. On the other hand, a significant difference was found in the serum cholesterol level between the SPI-P and SPI or SPI-T groups but not between the SPI and SPI-T groups. A similar tendency was observed for serum GPT and alkaline phosphatase activities, although there were no significant differences among dietary groups in small intestinal enzyme activities. As for the atherogenic index being a risk factor inducing atherosclerosis, the order of its value was SPI-P less than SPI less than SPI-T.
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PMID:Effect of feeding peptic digest of soy protein isolate on rat serum cholesterol. 310 Jul 38

The point and single electrode voltage clamp methods have been used to study the characteristics of junctional currents in Drosophila melanogaster larvae muscle fibers and the modulation of these currents by excitatory amino acids, short and long chain n-alkanols, and pentobarbital. The decay phase of junctional currents in Drosophila was found to be dominated by cooperativity in transmitter binding associated with reverberation, that is, repeated binding of transmitter with receptors as the transmitter molecules diffuse away from the active region. The current decay does not directly reflect the closure of ion channels and is qualitatively similar to the decay of miniature end-plate currents at the mouse neuromuscular junction after poisoning of acetylcholinesterase by paraoxon. In Drosophila an increase in membrane hyperpolarization both slows the time course of current decay and increases the degree of reverberation. The application of excitatory amino acids including glutamate, N-methyl-D-aspartate, quisqualate, and kainate causes a significant decrease in the amplitude of the junctional currents, a prolongation of the decay time course, and a reduction in reverberation of transmitter. The height of junctional currents is also diminished by the n-alkanols ethanol, pentanol, and octanol and by the barbiturate pentobarbital; ethanol also hastened the time course of decay of the currents.
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PMID:A voltage clamp study of the glutamate responsive neuromuscular junction in Drosophila melanogaster. 313 65


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