Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of cholinergic and GABAergic neuronal systems on the cycloheximide (CXM)-induced amnesia was investigated using the step-down-type passive avoidance task in mice. CXM (7.5-120 mg/kg, SC) given just after the training caused amnesia (indicated by short latency to step down from the platform on the grid floor) in the retention test conducted 24 hr later in a dose-dependent fashion. In the CXM (60 mg/kg)-treated mice, a choline esterase inhibitor, physostigmine (PHY; 0.125 and 0.25 mg/kg, IP), or GABA agonists, muscimol (1 and 2 mg/kg, IP) and baclofen (6 and 12 mg/kg, IP), given just after training markedly prolonged step down latency (SDL), indicating reversal of amnesia. The antiamnesic action of PHY (0.125 mg/kg) was almost completely antagonized by a central acetylcholine antagonist, scopolamine (3 mg/kg, SC), but not by a peripheral acetylcholine antagonist, butylscopolamine (3 mg/kg, SC). Furthermore, the antiamnesic action of muscimol (2 mg/kg) was reversed by GABA antagonists, picrotoxin (0.5 mg/kg, SC) and bicuculline (0.5 mg/kg, SC), while the effect of baclofen (12 mg/kg) was reversed by picrotoxin (0.5 mg/kg), but not by bicuculline (0.5 mg/kg). These results suggest that the dysfunction of cholinergic and GABAergic neuronal systems play an important role in the CXM-induced memory impairment on the passive avoidance task.
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PMID:Role of cholinergic and GABAergic neuronal systems in cycloheximide-induced amnesia in mice. 285 64

5 mg/kg mipafox [N,N'-bis(1-methylethyl)phosphordiamidic fluoride] was administered s.c. daily for 60 days in rats. The animals developed motor dysfunction-muscle twitchings, fasciculations and slight ataxia towards the end of the experimental period; the motor dysfunction was accompanied by neurochemical changes in the corpus striatum which included significantly reduced levels of cholinesterase, neurotoxicesterase, dopamine and GABA. The neurochemical imbalance in the corpus striatum may be related to motor dysfunction in mipafox-treated animals.
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PMID:Striatal neurochemical changes and motor dysfunction in mipafox-treated animals. 285 6

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

CSF neurotransmitter markers may reflect neurochemical alterations in Alzheimer's disease (AD). The best studied neurochemical deficit in AD is that of acetylcholine. Both acetylcholinesterase and butyrylcholinesterase activity have been reported to be reduced in some but not all studies of AD CSF. Studies of monoamine metabolites have also been controversial but most authors have found reduced concentrations of CSF HVA, lesser reductions in HIAA and no change in MHPG. CSF GABA concentrations have been found to be reduced in AD. Studies of CSF neuropeptides in AD have shown reduced concentrations of somatostatin and vasopressin, normal concentrations of vasoactive intestinal polypeptide and either normal or decreased concentrations of beta-endorphin and corticotropin releasing factor. Although no individual CSF neurochemical markers are specific for AD it may be possible to develop a profile of several neurochemical markers which will have enhanced specificity.
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PMID:CSF neurotransmitter markers in Alzheimer's disease. 287 17

The present investigation revealed the effect of the organochlorine insecticide dieldrin at the dose level 0.25 LD50 at different time intervals on the concentration of 11 rat brain amino acids, on the activities of glutamic oxyacetic transaminase (GOT), glutamic pyruvic transaminase (GpT) and cholinesterase. The study was also extended to include the total protein content during the tested periods. The daily injection of dieldrin caused a marked decrease in the levels of glutamic acid, glutamine and taurine and an increase in the levels of aspartic acid, asparagine, GABA, glycine, lysine, serine, alanine and histidine. However, the maximal increase and decrease were recorded for most of the tested amino acids at the end of the tested period. The activity of the transaminases increased significantly. The recorded values of GOT were usually higher than GPT. Cholinesterase activity was inhibited thoroughly during all the experimental periods. Total protein content was decreased in the experiment; the minimal value was given 3 days after the injection.
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PMID:Effect of dieldrin injection on the level of certain amino acids and some enzymes in rat brain. 287 4

Monocularly deprived (MD) cats show a loss of responsiveness to visual stimulation of the deprived eye among visual cortical neurons. Several lines of evidence suggest that this effect involves, at least in part, a suppression of deprived eye input, possibly mediated by GABA inhibition. In order to better understand the nature of this suppression we have evaluated the effectiveness of different types of disinhibitory and excitatory agents to reverse the effects of MD. We investigated bicuculline (a GABA antagonist); picrotoxin (a GABA antagonist with a different mechanism of action from bicuculline); strychnine (a glycine antagonist); ammonium ion (a blocker of membrane chloride channels); physostigmine (a cholinesterase inhibitor); and naloxone (an opiate antagonist and also a GABA antagonist). All drugs were given intravenously. Bicuculline restored binocularity to 50% of the visual cortical neurons tested and naloxone to 36%. With both drugs, receptive fields of the normal eye tended to lose specificity. The emergent deprived eye receptive fields were usually similar to those of the normal eye after drug administration. Ammonium ion produced binocular responses in 27% of neurons tested, but receptive fields were grossly abnormal; moreover, ammonium infusion tended to depress neuronal responsiveness. All other drugs tested failed to restore binocularity. These experiments lend further credence to the hypothesis that GABA inhibition contributes to the cortical effects of MD, since only drugs with GABA antagonistic action were effective in restoring neuronal responsiveness to the deprived eye.
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PMID:Comparative pharmacological effects on visual cortical neurons in monocularly deprived cats. 299 1

Rats were administered the organophosphorus insecticide acephate at 1.0 or 10.0 mg/kg.day for 15 weeks. Blood and brain samples were collected at the end of the treatment and analyzed for cholinesterase, acetylcholinesterase, and glutamic acid decarboxylase activities and catecholamine and amino acid levels. No significant inhibition in the activity of brain AChE was noted at doses of 1.0 or 10.0 mg/kg.day. Low levels of acephate exposure (1.0 mg/kg.day), which did not alter plasma cholinesterase or RBC acetylcholinesterase activity levels, resulted in a significant elevation of plasma epinephrine and norepinephrine levels. Decreased GABA, dopamine, and tyrosine levels and glutamic acid decarboxylase activity were observed in brains of these rats. Similar changes occurred in rats exposed to 10 mg of acephate/kg.day; however, plasma cholinesterase and RBC acetylcholinesterase activities were inhibited. These observations suggest that chronic exposure to acephate altered the activity of the noncholinergic system without altering the cholinergic activity, and that low-level chronic exposure to organophosphorous compounds cannot be predicted by measuring the ChE or AChE enzyme activities.
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PMID:Neurotoxic effects of low-level chronic acephate exposure in rats. 360 37

Some enzymatic parameters of neuronal transmission as well as the occurrence and the properties or carboxylic ester hydrolases in the hippocampal region of the wistar rat are investigated by histochemical and comparable biochemical methods. The acetylcholinesterase-, the monoamine oxidase- and the GABA-transaminase reaction are found at fibre structures, the course of which is seen more or less clearly. The histochemical picture of these enzymes is very different in each hippocampal layer and mainly limited by the corresponding number of reacting fibres. The origin and attribution of the fibres to the afferent and efferent systems are discussed. The occurrence of the acetylcholinesterase, the monoamine oxidase and the GABA-transferase as well as of the biogenic amines and the GABA are hints for the existence of cholinergic as well as aminergic and GABA-ergic processes of transmission in the hippocampal region. In the hippocampal region, the cingular and the optic cortex carboxylic ester hydrolases acetylcholinesterase, unspecific cholinesterase and the A-, B- and C-esterase could be demonstrated. The acetylcholinesterase of the hippocampal region is for the most part firmly membrane-bound and exists at least in two multiple, formalin-sensitive forms which are histochemically located in fibre structures. The unspecific cholinesterase, localized in the hippocampal region within vessel and capillary walls, exists in an electrophoretic mobile, formalin-sensitive form. Nearly half of the enzymes is soluble. A preferred binding to definite cell organelles was not demonstrable. In the hippocampal region the 3 multiple forms of the A-esterase are formalin-instable lyoenzymes. Good solubility and high formalin-sensitivity are the reason, why A-esterases are not demonstrable with usually histochemical methods. In the hippo ampal region the B-esterase is tightly bound to n electrophoretic mobile formalin-sensitive form in the microsomal fraction. In the cytoplasm of the neurones the desmoenzyme appears more or less granular. The 3 multiple forms of the C-esterase are formalin-sensitive to a different degree. Good solubility and low formalin-sensitivity, compared to the A-esterases are responsible for the fact, that the C-esterases can be shown histochemically only after en-bloc-fixation. The reaction products are granular. The similar behaviour of C-esterase and acid phosphatase, stated by many tests, suggests the C-esterases of the B- and C-type results in the same reactivity of pyramidal and granular cells of the hippocampal region. Some small, very strongly reacting cells belong to other cell types (probably basket cells or polymorphic cells).
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PMID:[Histochemical and biochemical investigations of the hippocampus and neocortex of the Wistar rat. I. Carboxylic ester hydrolases, transmitter enzymes and transmitters of the normal animal (author's transl)]. 610 39

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

Benzodiazepines (BDZ) interact with specific receptors (R), whose activation improves Cl- -channel gating by the GABA receptor (GABA-R). Neurones, whose GABAergic input has a certain level of activity, will be more inhibited in the presence of BDZ (primary target neurones for BDZ). Secondarily, neurones dependent on the activity of primary target neurones will also be effected. Drugs that interact with GABAergic functions (except the BDZ-R) or with the function of primary or secondary target neurones may inhibit some or all BDZ effects; these are nonspecific BDZ antagonists (e.g. GABA-antagonists, cholinesterase inhibitors, naloxone, methylxanthines). Specific BDZ antagonists inhibit the action of BDZ by blocking competitively the BDZ-R. Ro 15-1788 is the best investigated specific BDZ antagonist. Virtually devoid of any pharmacological action by itself, the compound blocks all typical effects of BDZ. It is well tolerated also in man and will find application in anaesthesiology to shorten the sedative and muscle relaxant effect of BDZ and in emergency services to reverse comatose states after BDZ overdosage. Recently drugs have been found that produce effects opposite to the BDZ tranquilizers by inducing a conformation of the BDZ-R which depresses GABA-mediated Cl- -channel gating. The effects of these inverse agonists (e.g. proconvulsant , convulsant, anxiogenic) are blocked by pure competitive BDZ-R blockers, such as Ro 15-1788.
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PMID:Antagonists of benzodiazepines. 614 9


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