| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| T Kosasa, Y Kuriya, K Matsui, Y Yamanish. Effect of donepezil hydrochloride (E2020) on basal concentration of extracellular acetylcholine in the hippocampus of rats. European journal of pharmacology. vol 380. issue 2-3. 1999-11-01. PMID:10513568. |
the effects of oral administration of the centrally acting acetylcholinesterase (ache) inhibitors, donepezil hydrochloride (donepezil: e2020: (+/-)-2-[(1-benzylpiperidin-4-yl)methyl]-5,6-dimethoxy-indan-1-one monohydrochloride), tacrine (9-amino-1,2,3,4-tetrahydroacridine hydrochloride) and ena-713 (rivastigmine: (s)-n-ethyl-3-[(1-dimethyl-amino)ethyl]-n-methyl-phenylcarbamate hydrogentartrate), which have been developed for the treatment of alzheimer's disease, on the extracellular acetylcholine concentration in the hippocampus of rats were evaluated by using a microdialysis technique without adding cholinesterase inhibitor to the perfusion solution. |
1999-11-01 |
2023-08-12 |
rat |
| T Kosasa, Y Kuriya, K Matsui, Y Yamanish. Effect of donepezil hydrochloride (E2020) on basal concentration of extracellular acetylcholine in the hippocampus of rats. European journal of pharmacology. vol 380. issue 2-3. 1999-11-01. PMID:10513568. |
these results suggest that oral administration of donepezil, tacrine and ena-713 increases acetylcholine concentration in the synaptic cleft of the hippocampus mostly through ache inhibition, and that donepezil has a more potent activity than tacrine and a longer-lasting effect than ena-713 on the central cholinergic system. |
1999-11-01 |
2023-08-12 |
rat |
| D Grisaru, M Sternfeld, A Eldor, D Glick, H Sore. Structural roles of acetylcholinesterase variants in biology and pathology. European journal of biochemistry. vol 264. issue 3. 1999-10-14. PMID:10491113. |
apart from its catalytic function in hydrolyzing acetylcholine, acetylcholinesterase (ache) affects cell proliferation, differentiation and responses to various insults, including stress. |
1999-10-14 |
2023-08-12 |
human |
| D I Mitsur. [Changes of the aluminum and silicon contents and cholinergic activity of the blood depending on the course of the gastroduodenal ulcer]. Klinichna khirurhiia. issue 5. 1999-09-08. PMID:10429395. |
in 37 patients with gastroduodenal ulcer disease were revealed the changes of concentration of aluminium and silicon in blood, of acetylcholine in erythrocytes and plasma, the cholinesterase (ache) activity depending on the disease clinical course, the ulcer size; the interconnection between the blood cholinergic activity and the contents of aluminium and silicon; the influence of aluminium and silicon ions on the ache activity of plasma and erythrocytes, what is confirmed by the correlational analysis data and gives and arguments for application of chemical compounds with aluminium and silicon in treatment and prophylaxis of an ulcer disease recurrence. |
1999-09-08 |
2023-08-12 |
Not clear |
| C A Nurse, M Zhan. Acetylcholine contributes to hypoxic chemotransmission in co-cultures of rat type 1 cells and petrosal neurons. Respiration physiology. vol 115. issue 2. 1999-08-27. PMID:10385033. |
recent evidence has strengthened the case for acetylcholine (ach) as a co-released transmitter: (i) cultured type 1 cells express several cholinergic markers including the vesicular ach transporter (vacht), intracellular acetylcholinesterase (ache), and occasional clear cored vesicles (approximately 50 nm diameter); (ii) the frequency of spontaneous synaptic activity, as well as the hypoxia-induced depolarization recorded in 'juxtaposed' pn in co-culture, were partially suppressed by the nicotinic ach receptor (nachr) blocker, mecamylamine (2 microm); (iii) consistent with the presence of extracellular ache, ach-mediated membrane noise in type 1 cells as well as the hypoxia-evoked pn response in co-culture were potentiated in a few cases by the ache inhibitor, eserine (100 microm). |
1999-08-27 |
2023-08-12 |
rat |
| D Kaufer, A Friedman, S Seidman, H Sore. Anticholinesterases induce multigenic transcriptional feedback response suppressing cholinergic neurotransmission. Chemico-biological interactions. vol 119-120. 1999-08-19. PMID:10421471. |
cholinesterase inhibitors (anti-ches) include a wide range of therapeutic, agricultural and warfare agents all aimed to inhibit the catalytic activity of the acetylcholine (ach) hydrolysing enzyme acetylcholinesterase (ache). |
1999-08-19 |
2023-08-12 |
mouse |
| B D Banerjee, V Seth, A Bhattacharya, S T Pasha, A K Chakrabort. Biochemical effects of some pesticides on lipid peroxidation and free-radical scavengers. Toxicology letters. vol 107. issue 1-3. 1999-07-29. PMID:10414779. |
acetylcholine esterase (ache), gamma glutamyl transpeptidase (ggt) and gsh level were also assayed in lymphocytes. |
1999-07-29 |
2023-08-12 |
human |
| K Tuovinen, E Kaliste-Korhonen, F M Raushel, O Hännine. Success of pyridostigmine, physostigmine, eptastigmine and phosphotriesterase treatments in acute sarin intoxication. Toxicology. vol 134. issue 2-3. 1999-07-26. PMID:10403635. |
the acute toxicity of organophosphorus (op) compounds in mammals is due to their irreversible inhibition of acetylcholinesterase (ache) in the nervous system, which leads to increased synaptic acetylcholine levels. |
1999-07-26 |
2023-08-12 |
mouse |
| H B Peng, H Xie, S G Rossi, R L Rotund. Acetylcholinesterase clustering at the neuromuscular junction involves perlecan and dystroglycan. The Journal of cell biology. vol 145. issue 4. 1999-07-21. PMID:10330416. |
prelabeling ache on the surface of xenopus muscle cells revealed that preexisting ache molecules could be recruited to form clusters that colocalize with acetylcholine receptors at sites of nerve-muscle contact. |
1999-07-21 |
2023-08-12 |
xenopus_laevis |
| S Olivera, D Rodriguez-Ithurralde, J M Henle. Acetylcholinesterase potentiates [3H]fluorowillardiine and [3H]AMPA binding to rat cortical membranes. Neuropharmacology. vol 38. issue 4. 1999-07-02. PMID:10221754. |
in addition to its action at cholinergic synapses acetylcholinesterase (ache) has been proposed to modulate neuronal activity by mechanisms unrelated to the hydrolysis of acetylcholine. |
1999-07-02 |
2023-08-12 |
rat |
| G Feng, E Krejci, J Molgo, J M Cunningham, J Massoulié, J R Sane. Genetic analysis of collagen Q: roles in acetylcholinesterase and butyrylcholinesterase assembly and in synaptic structure and function. The Journal of cell biology. vol 144. issue 6. 1999-06-14. PMID:10087275. |
at the skeletal neuromuscular junction, asymmetric ache is anchored to the basal lamina of the synaptic cleft, where it hydrolyzes acetylcholine to terminate synaptic transmission. |
1999-06-14 |
2023-08-12 |
mouse |
| M Hilgert, M Nöldner, S S Chatterjee, J Klei. KA-672 inhibits rat brain acetylcholinesterase in vitro but not in vivo. Neuroscience letters. vol 263. issue 2-3. 1999-06-10. PMID:10213168. |
however, when we employed the microdialysis procedure to monitor acetylcholine (ach) release from rat hippocampus, no effect of ka-672 (0.1-10 mg/kg) was found, indicating a lack of inhibition of brain ache under in vivo-conditions. |
1999-06-10 |
2023-08-12 |
rat |
| C N Pop. Organophosphorus pesticides: do they all have the same mechanism of toxicity? Journal of toxicology and environmental health. Part B, Critical reviews. vol 2. issue 2. 1999-05-18. PMID:10230392. |
it is concluded that all op anticholinesterases potentially have a mechanism of toxicity in common, that is, phosphorylation of ache causing accumulation of acetylcholine, overstimulation of cholinergic receptors, and consequent clinical signs of cholinergic toxicity. |
1999-05-18 |
2023-08-12 |
Not clear |
| G Testylier, N Micoud, S Martinez, G Lallemen. Simultaneous in vivo determination of acetylcholinesterase activity and acetylcholine release in the cortex of waking rat by microdialysis. Effects of VX. Journal of neuroscience methods. vol 81. issue 1-2. 1999-05-12. PMID:9696310. |
we have designed a microdialysis technique to measure acetylcholinesterase (ache) activity in the cortex of freely moving rats while simultaneously measuring the release of acetylcholine (ach). |
1999-05-12 |
2023-08-12 |
rat |
| J E Keymer, J Gaete, G Kameid, J Alvare. Acetylcholinesterase and inhibitors: effects upon normal and regenerating nerves of the rat. The European journal of neuroscience. vol 11. issue 3. 1999-04-26. PMID:10103097. |
in peripheral nerves, the function of acetylcholinesterase (ache) is not related to hydrolysis of acetylcholine. |
1999-04-26 |
2023-08-12 |
rat |
| J Dudel, M Heckman. Desensitization reduces amplitudes of quantal end-plate currents after a single preceding end-plate current in mouse muscle. Pflugers Archiv : European journal of physiology. vol 437. issue 4. 1999-04-23. PMID:10089570. |
twenty milliseconds after an epc, a subsequent qepc was reduced to 90% of control, and to 70-80% if acetylcholine esterase (ache) was blocked. |
1999-04-23 |
2023-08-12 |
mouse |
| A Morett. Experimental and clinical toxicology of anticholinesterase agents. Toxicology letters. vol 102-103. 1999-02-25. PMID:10022304. |
their acute toxic effect in the central and peripheral nervous system is due to inhibition of acetylcholinesterase (ache) at nerve endings which causes accumulation of acetylcholine and consequently overstimulation of the nicotinic and muscarinic receptors. |
1999-02-25 |
2023-08-12 |
Not clear |
| T Szegletes, W D Mallender, P J Thomas, T L Rosenberr. Substrate binding to the peripheral site of acetylcholinesterase initiates enzymatic catalysis. Substrate inhibition arises as a secondary effect. Biochemistry. vol 38. issue 1. 1999-02-18. PMID:9890890. |
however, our analyses indicate that the primary physiologic role of the ache peripheral site is to accelerate the hydrolysis of acetylcholine at low substrate concentrations. |
1999-02-18 |
2023-08-12 |
Not clear |
| J McFerrin, W K Engel, V Askana. Impaired innervation of cultured human muscle overexpressing betaAPP experimentally and genetically: relevance to inclusion-body myopathies. Neuroreport. vol 9. issue 14. 1999-01-20. PMID:9831451. |
innervated normal cultured muscle fibers were continuously contracting and fully cross-striated, and they had acetylcholine receptors (achrs) and acetylcholinesterase (ache) accumulated only at the neuromuscular junctions (nmjs). |
1999-01-20 |
2023-08-12 |
human |
| R M Nitsch, S Rossner, C Albrecht, M Mayhaus, J Enderich, R Schliebs, M Wegner, T Arendt, H von der Kamme. Muscarinic acetylcholine receptors activate the acetylcholinesterase gene promoter. Journal of physiology, Paris. vol 92. issue 3-4. 1999-01-13. PMID:9789819. |
the results suggest a feedback mechanism by which the ache gene is activated by cholinergic neurotransmission, possibly leading to increased formation of ache protein and accelerated degradation of acetylcholine at cholinergic synapses. |
1999-01-13 |
2023-08-12 |
human |