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)

Monosodium-L-glutamate given subcutaneously to pregnant rats caused acute necrosis of the acetylcholinesterase-positive neurons in the area postrema. The same effect has been observed in the area postrema of fetal rats. The process of neuronal cell death and the elimination of debris by microglia cells proved to be similar in pregnant animals and in their fetuses. However, embryonal neurons were more sensitive to glutamate as judged by the rapidity of the process and the dose-response relationship. These observations raise the possibility of transplacental poisoning in human fetuses after the consumption of glutamate-rich food by the mother.
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PMID:Neurotoxicity of monosodium-L-glutamate in pregnant and fetal rats. 343 10

Purified human erythrocyte acetylcholinesterase was labeled by reductive radiomethylation with saturating amounts of [14C]formaldehyde and sodium cyanoborohydride. Acid hydrolysis and automated amino acid analysis permitted both identification of radiomethylated components by their coelution with radiomethylated standards and quantitation of these components. The methylated N-terminal amino acids glutamate and arginine were observed at levels of 0.66 and 0.34 residues, respectively, per 70-kilodalton subunit, and lysine residues were methylated on their epsilon-amino groups to a level of 7.40 residues per subunit [Haas, R., & Rosenberry, T.L. (1985) Anal. Biochem. 148, 154-162]. In addition, each subunit contained 1.35 residues of methylated ethanolamine and 0.98 residue of methylated glucosamine. Papain digestion cleaved the intact enzyme into two fragments, an enzymatically active hydrophilic fragment and a small hydrophobic fragment that represented the membrane-binding domain. The radiomethylated amino acids were quantitatively retained in the hydrophilic fragment, while the methylated ethanolamine and glucosamine were confined exclusively to the hydrophobic domain fragment. This fragment included the C-terminal dipeptide of the subunit. Peptide sequencing by manual Edman methods was combined with radiomethylation to demonstrate the sequence His-Gly-ethanolamine-Z for the hydrophobic domain fragment. The ethanolamine residue in this sequence is in amide linkage to the C-terminal Gly and is clearly distinct from the ethanolamine residues in Z which are susceptible to radiomethylation in the intact enzyme. Since Z also includes glucosamine and 2 mol of fatty acids [Roberts, W.L. & Rosenberry, T.L. (1985) Biochem. Biophys. Res. Commun. 133, 621-627], we conclude that the membrane-binding domain of human erythrocyte acetylcholinesterase is a covalently linked glycolipid at the C-termini of the subunits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Identification of amine components in a glycolipid membrane-binding domain at the C-terminus of human erythrocyte acetylcholinesterase. 352 71

Extracellular amino acid levels in the rat piriform cortex, an area highly susceptible to seizure-induced neuropathology, were determined by means of intracranial microdialysis. Seizures were induced by systemic administration of either soman (O-1,2,2-trimethylpropyl methylphosphonofluoridate), a potent inhibitor of acetylcholinesterase, or the excitotoxin kainic acid. Extracellular glutamate levels increased in animals with seizures shortly after administration of either convulsant, but this change was statistically significant only in the case of soman-treated animals. Extracellular taurine levels increased markedly, reaching two- and fourfold baseline levels during the second hour of soman- and kainic acid-induced seizures, respectively. Taurine levels did not increase in the subpopulation of soman-treated animals without seizures, a finding indicating that elevation of extracellular taurine level is seizure related. Thus, we propose that taurine efflux may be a physiological cellular response to neuronal changes produced by excitotoxic chemicals, either directly or as a consequence of seizures.
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PMID:Changes in extracellular amino acids during soman- and kainic acid-induced seizures. 359 90

Studied was the enzyme constellation, resp., activity of alkaline phosphatase (AP), glutamate-oxaloacetic transaminase (GOT), glutamate-pyruvate transaminase (GPT), aldolase (ALD), leucin-aminopeptidase (LAP), cholinesterase (CE), creatine phosphokinase (CPK), lactate dehydrogenase (LDH), ornithine carbamoyltransferase (OCT), and guanase (G) in a total of 360 clinically normal and lactating and dry cows of the Black-and-White and Simmental crossbreeds. Characteristic quantitative changes were found with GOT, GPT, ALD, LDH, and CPK both over the dry period and over the entire period of lactation. The activity of LAP, AP, OCT, and G was not influenced by the functional status of the animals. In the course of the analyses there were changes in the serum ALD, CE, and GOT, associated with the breed. The enzymes referred to were studied with a view to establishing their normal parameters needed for the practice as the base to demonstrate preclinical disturbances in individual organs and tissues of the cows during pregnancy and the puerperium.
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PMID:[Enzyme constellation in cows of the Simmental crossbreed and Black Pied breed during the dry period and lactation]. 367 21

It is well established that the putative excitatory neurotransmitters, glutamate (Glu) and aspartate (Asp), are neurotoxins that have the potential of destroying central neurons by an excitatory mechanism. Kainic acid (KA), a rigid structural analog of Glu, powerfully reproduces the excitatory neurotoxic (excitotoxic) action of Glu on central neurons and, in addition, causes sustained limbic seizures and a pattern of seizure-linked brain damage in rats that closely resembles that observed in human epilepsy. In the course of studying the seizure-related brain damage syndrome induced by KA, we observed that a similar type of brain damage occurs as a consequence of sustained seizure activity induced by any of a variety of methods. These included intraamygdaloid or supradural administration of known convulsants such as bicuculline, picrotoxin and folic acid, or systemic administration of lithium and cholinergic agonists or cholinesterase inhibitors that have not commonly been viewed as convulsants. We have further observed that this type of brain damage can be reproduced in the hippocampus by persistent electrical stimulation of the perforant path, a major excitatory input to the hippocampus that is thought to use Glu as transmitter. It is a common feature of all such neurotoxic processes that the acute cytopathology resembles the excitotoxic type of damage induced by Glu or Asp, which is acute swelling of dendrites and vacuolar degeneration of neuronal soma, without acute changes in axons or axon terminals. We have found that the seizure-brain damage syndrome induced by cholinergic agents can be prevented by pretreatment with atropine and that the syndrome induced by any of the above methods, cholinergic or noncholinergic, can be either prevented or aborted respectively by either pre-or posttreatment with diazepam. Our findings in experimental animals may be summarized in terms of their potential relevance to human epilepsy as follows. Sustained complex partial seizure activity consistently results in cellular damage if allowed to continue for longer than 1 hr. Hippocampal, or Ammon's horn, sclerosis is the primary pathological result. It may be a priority goal, therefore, in the management of human epilepsy to control such seizure activity within very narrow limits. This proposal is discussed in terms of three major transmitter systems that may be involved; cholinergic, GABAergic, and glutamergic/aspartergic. The cholinergic system may play a role in generating or maintaining this type of seizure activity, and anticholinergics may protect against it provided they are given prior to commencement of behavioral seizures.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Excitotoxic mechanisms of epileptic brain damage. 370 27

The rat brains homogenized with different media (sucrose, ethylene glycol, dimethyl sulfoxide and urea) yielded different amounts of microsomal fractions. The dielectric constant, density and viscosity of the homogenization media did not correlate with the amount of microsomes separated by differential centrifugation. The homogenization media containing dimethyl sulfoxide were the most efficient for the isolation of rat brain microsomes. The increase in the yield was up to 4-fold when 50% (v/v) dimethyl sulfoxide was employed. Microsomes isolated in this manner were analogous to those obtained from isotonic sucrose solution, as was demonstrated by their chemical and enzymatic (5'-nucleotidase, adenosine deaminase, guanine deaminase, purine-nucleoside phosphorylase, lactate, malate and glutamate dehydrogenases, amine oxidase fumarate hydratase, acid and alkaline phosphatase, acetylcholinesterase, NADPH-cytochrome c reductase, catalase and thiamine-diphosphatase) characterization.
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PMID:An improved method for the preparation of rat brain microsomes. 371 74

Adult male rats have lower serum cholinesterase activity levels than adult female rats and hypophysectomized male rats have higher activity levels than sham-operated males (similar to control females). GH administered to hypophysectomized male rats abolishes the effect of hypophysectomy on serum cholinesterase. Adult male rats treated neonatally with monosodium L-glutamate to induce arcuate nucleus lesions of the hypothalamus have higher serum cholinesterase activities and decreased serum GH concentrations. GH administered to these male rats results in decreased serum cholinesterase activities. These experiments demonstrate that GH is a negative modulator of serum cholinesterase in the male rat.
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PMID:Growth hormone modulates serum cholinesterase. 394 77

An increase in content of acetylcholine (AC) as well as stimulation of choline acetyltransferase and acetylcholinesterase were observed in basal ganglia of rat brain during development of alcohol dependency, thus indicating the activation of the AC structures. Less distinct activation of the AC structures occurred in limbic (frontal) cortex. At the step of complete alcohol dependency the patterns of AC metabolism were considerably normalized in the both brain structures; at the same time, activity of the gamma-aminobutyric acid (GABA) system was decreased, which occurred due to inhibition of the GABA synthesis. At the III step of experimental alcoholism with "physical" dependency on ethanol synthesis and release of the AC were lowered, especially distinct in basal ganglia. These phase alterations in the activity of the AC structures in basal ganglia were accompanied by the similar alterations in content of glutamate: an increase of glutamate at the I step of alcoholism and a decrease--at the III step. Possible mechanisms and pathogenetic role of the phase alterations observed in metabolism of the brain neurotransmitters and in activity of AC- and GABA-structures during development of alcohol dependency are discussed. The data obtained suggest that the specific steps of alcoholism should be taken into consideration in the differential treatment using neurotransmitter drugs.
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PMID:[Metabolism of acetylcholine and gamma-aminobutyric acid in the basal ganglia and limbic cortex of rats at different stages in the development of alcohol dependence]. 395 3

1. The dorsal lateral geniculate nucleus (LGN) of the cat stains densely for acetylcholinesterase, which is present in intra-axonal and extracellular locations.2. Acetylcholine (ACh), cholinomimetic drugs, anticholinesterases and ACh antagonists were administered iontophoretically to neurones in the LGN.3. ACh excited eighty-six of 184 (46.7%) geniculate neurones and depressed seven (3.8%).4. The excitatory response to ACh was frequently larger than that to L-glutamate and had a comparable time course.5. There was a considerable variation in the proportion of ACh sensitive cells in different animals. ACh firing was facilitated by optic nerve or visual stimulation.6. Carbamylcholine was the most active of the choline esters tested, frequently exceeding ACh in potency. The other choline esters and nicotine were consistently less active than ACh.7. Anticholinesterases, eserine, neostigmine and edrophonium potentiated the action of ACh, and often caused excitation. Eserine caused an initial small enhancement in the amplitude of the focal potential evoked by optic nerve stimulation followed by a reduction in amplitude and prolongation of duration of the potential.8. Atropine and benzoquinonium effectively prevented the ACh excitation of many cells. Dihydro-beta-erythroidine failed to cause a significant reduction in the magnitude of the ACh response. All three ACh antagonists failed to reduce the excitant effects of optic nerve or visual stimulation.9. Stimulation of the mesencephalic reticular formation caused either an enhancement or a reduction in the excitability of ACh sensitive neurones in the LGN. Benzoquinonium abolished the excitatory effects of reticular formation stimulation.10. The findings presented in this paper suggest that ACh is the transmitter released by terminals of nerves of the reticular formation projection to the LGN.
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PMID:A study of cholinoceptive cells in the lateral geniculate nucleus. 429 88

The tonic flexor muscles of the crayfish abdomen respond with a large depolarizing potential to acetylcholine iontophoresed onto a neuromuscular Junction, but not to glutamate. Excitatory junctional potentials are abolished by d-tubocurarine and enhanced by a cholinesterase inhibitor. The membrane is depolarized and the junctional potentials are desensitized by excess acetylcholine. Thus acetylcholine is thought to be the neuromuscular transmitter.
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PMID:Acetylcholine: possible neuromuscular transmitter in Crustacea. 433 82


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