Database : MEDLINE
Search on : D02.675.276.046 [DeCS Category]
References found : 102 [refine]
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  1 / 102 MEDLINE  
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PMID:27373830
Author:Mamaligas AA; Ford CP
Address:Department of Neurosciences, Case Western Reserve University School of Medicine, 10900 Euclid Ave., Cleveland, OH 44106-4970, USA.
Title:Spontaneous Synaptic Activation of Muscarinic Receptors by Striatal Cholinergic Neuron Firing.
Source:Neuron; 91(3):574-86, 2016 Aug 03.
ISSN:1097-4199
Country of publication:United States
Language:eng
Abstract:Cholinergic interneurons (CHIs) play a major role in motor and learning functions of the striatum. As acetylcholine does not directly evoke postsynaptic events at most striatal synapses, it remains unclear how postsynaptic cholinergic receptors encode the firing patterns of CHIs in the striatum. To examine the dynamics of acetylcholine release, we used optogenetics and paired recordings from CHIs and medium spiny neurons (MSNs) virally overexpressing G-protein-activated inwardly rectifying potassium (GIRK) channels. Due to the efficient coupling between endogenous muscarinic receptors and GIRK channels, we found that firing of individual CHIs resulted in monosynaptic spontaneous inhibitory post-synaptic currents (IPSCs) in MSNs. Paired CHI-MSN recordings revealed that the high probability of acetylcholine release at these synapses allowed muscarinic receptors to faithfully encode physiological activity patterns from individual CHIs without failure. These results indicate that muscarinic receptors in striatal output neurons reliably decode CHI firing.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Cholinesterase Inhibitors); 0 (Receptor, Muscarinic M4); 51FOB87G3I (Ambenonium Chloride); N9YNS0M02X (Acetylcholine)


  2 / 102 MEDLINE  
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PMID:26586471
Author:Draczkowski P; Tomaszuk A; Halczuk P; Strzemski M; Matosiuk D; Jozwiak K
Address:Faculty of Pharmacy, Medical University of Lublin, ul. Chodzki 4a, 20-093 Lublin, Poland.
Title:Determination of affinity and efficacy of acetylcholinesterase inhibitors using isothermal titration calorimetry.
Source:Biochim Biophys Acta; 1860(5):967-974, 2016 May.
ISSN:0006-3002
Country of publication:Netherlands
Language:eng
Abstract:BACKGROUND: Acetylcholinesterase (AChE), an enzyme rapidly terminating nerve signals at synapses of cholinergic neurons is an important drug target in treatment of Alzheimer's disease and related memory loss conditions. Here we present comprehensive use of isothermal titration calorimetry (ITC) for investigation of AChE kinetics and AChE-inhibitor interactions. METHODS: Acetylcholinesterase (AChE, EC 3.1.1.7) from Electrophorus electricus was assayed for interactions with five well known AChE inhibitors, galanthamine, tacrine, donepezil, edrophonium and ambenonium. In ITC experiments the inhibitors were injected to the enzyme solution solely (for thermodynamic characterization of binding) or in presence of the substrate, acetylcholine (for determination of inhibitors potency). RESULTS: Detailed description of various experimental protocols is presented, allowing evaluation of inhibitors potency (in terms of IC50 and Ki) and thermodynamic parameters of the binding. The potency of tested inhibitors was in nano to micromolar range which corresponded to activities determined in conventional method. Binding of all inhibitors showed to be enthalpy driven and obtained Ka values demonstrated good correlation with the data from standard Ellman's assay. CONCLUSIONS: Obtained results confirmed the usability of the ITC technique for comprehensive characterization of AChE-inhibitor interactions and AChE kinetics. The method reduced the complexity of reaction mixture and interference problems with the advantage of using natural substrates. GENERAL SIGNIFICANCE: The work reports complete thermodynamic characteristics of the AChE - inhibitor complexes. Due to the universal character of ITC measurements, described protocols can be easily adapted to other enzymatic systems.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Cholinesterase Inhibitors); 0 (Fish Proteins); 0 (Indans); 0 (Piperidines); 0D3Q044KCA (Galantamine); 4VX7YNB537 (Tacrine); 51FOB87G3I (Ambenonium Chloride); 70FP3JLY7N (Edrophonium); 8SSC91326P (donepezil); EC 3.1.1.7 (Acetylcholinesterase); N9YNS0M02X (Acetylcholine)


  3 / 102 MEDLINE  
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PMID:26697233
Author:Zuo ZX; Wang YJ; Liu L; Wang Y; Mei SH; Feng ZH; Wang M; Li XY
Address:Department of Neurosurgery, First Affiliated Hospital, Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China ; Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology an
Title:Huperzine A Alleviates Mechanical Allodynia but Not Spontaneous Pain via Muscarinic Acetylcholine Receptors in Mice.
Source:Neural Plast; 2015:453170, 2015.
ISSN:1687-5443
Country of publication:United States
Language:eng
Abstract:Chronic pain is a major health issue and most patients suffer from spontaneous pain. Previous studies suggest that Huperzine A (Hup A), an alkaloid isolated from the Chinese herb Huperzia serrata, is a potent analgesic with few side effects. However, whether it alleviates spontaneous pain is unclear. We evaluated the effects of Hup A on spontaneous pain in mice using the conditioned place preference (CPP) behavioral assay and found that application of Hup A attenuated the mechanical allodynia induced by peripheral nerve injury or inflammation. This effect was blocked by atropine. However, clonidine but not Hup A induced preference for the drug-paired chamber in CPP. The same effects occurred when Hup A was infused into the anterior cingulate cortex. Furthermore, ambenonium chloride, a competitive inhibitor of acetylcholinesterase, also increased the paw-withdrawal threshold but failed to induce place preference in CPP. Therefore, our data suggest that acetylcholinesterase in both the peripheral and central nervous systems is involved in the regulation of mechanical allodynia but not the spontaneous pain.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Alkaloids); 0 (Analgesics); 0 (Cholinesterase Inhibitors); 0 (Lipopolysaccharides); 0 (Muscarinic Antagonists); 0 (Receptors, Muscarinic); 0 (Sesquiterpenes); 0111871I23 (huperzine A); 51FOB87G3I (Ambenonium Chloride); 7C0697DR9I (Atropine); EC 3.1.1.7 (Acetylcholinesterase); MN3L5RMN02 (Clonidine)


  4 / 102 MEDLINE  
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PMID:25186736
Author:Petrov KA; Girard E; Nikitashina AD; Colasante C; Bernard V; Nurullin L; Leroy J; Samigullin D; Colak O; Nikolsky E; Plaud B; Krejci E
Address:COGNAC G, Université Paris Descartes, CNRS, Service de Santé des Armées, UMR 8257, MD 4, 75006 Paris, France, A.E. Arbuzov Institute of Organic and Physical Chemistry, Kazan 420088, Russia, Kazan Federal University, Kazan 420008, Russia.
Title:Schwann cells sense and control acetylcholine spillover at the neuromuscular junction by α7 nicotinic receptors and butyrylcholinesterase.
Source:J Neurosci; 34(36):11870-83, 2014 Sep 03.
ISSN:1529-2401
Country of publication:United States
Language:eng
Abstract:Terminal Schwann cells (TSCs) are key components of the mammalian neuromuscular junction (NMJ). How the TSCs sense the synaptic activity in physiological conditions remains unclear. We have taken advantage of the distinct localization of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) at the NMJ to bring out the function of different ACh receptors (AChRs). AChE is clustered by the collagen Q in the synaptic cleft and prevents the repetitive activation of muscle nicotinic AChRs. We found that BChE is anchored at the TSC by a proline-rich membrane anchor, the small transmembrane protein anchor of brain AChE. When BChE was specifically inhibited, ACh release was significant depressed through the activation of α7 nAChRs localized on the TSC and activated by the spillover of ACh. When both AChE and BChE were inhibited, the spillover increased and induced a dramatic reduction of ACh release that compromised the muscle twitch triggered by the nerve stimulation. α7 nAChRs at the TSC may act as a sensor for spillover of ACh adjusted by BChE and may represent an extrasynaptic sensor for homeostasis at the NMJ. In myasthenic rats, selective inhibition of AChE is more effective in rescuing muscle function than the simultaneous inhibition of AChE and BChE because the concomitant inhibition of BChE counteracts the positive action of AChE inhibition. These results show that inhibition of BChE should be avoided during the treatment of myasthenia and the pharmacological reversal of residual curarization after anesthesia.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Bungarotoxins); 0 (Cholinesterase Inhibitors); 0 (Membrane Proteins); 0 (Nerve Tissue Proteins); 0 (PRiMA1 protein, rat); 0 (alpha7 Nicotinic Acetylcholine Receptor); 51FOB87G3I (Ambenonium Chloride); EC 3.1.1.7 (Acetylcholinesterase); EC 3.1.1.8 (Butyrylcholinesterase); N8ONU3L3PG (Terbutaline); N9YNS0M02X (Acetylcholine); Y1850G1OVC (bambuterol)


  5 / 102 MEDLINE  
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PMID:24130994
Author:Yudin MA; Ivanov IM; Nikiforov AS; Kornyukhina TM; Tyunin MA
Address:Research and Testing Institute of Military Medicine, S. M. Kirov Military Medical Academy, St. Petersburg, Russia. mihei_bridge@mail.ru.
Title:Use of inclusion complex of cyclodextrin with ambenonium to improve the treatment of anticholinesterase poisoning.
Source:Bull Exp Biol Med; 155(2):218-20, 2013 Jun.
ISSN:1573-8221
Country of publication:United States
Language:eng
Abstract:The complex of ambenonium with methyl-ß-cyclodextrin injected intramuscularly to rats caused more pronounced inhibition of acetylcholinesterase in erythrocyte and brain than free drug. The use of this complex as part of combined therapy significantly reduces mortality in animals during experimental anticholinesterase poisoning in comparison with the controls.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Cholinesterase Inhibitors); 0 (Drug Combinations); 0 (beta-Cyclodextrins); 0 (methyl-beta-cyclodextrin); 51FOB87G3I (Ambenonium Chloride); EC 3.1.1.7 (Acetylcholinesterase)


  6 / 102 MEDLINE  
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PMID:23992036
Author:Perez XA; McIntosh JM; Quik M
Address:Center for Health Sciences, SRI International, Menlo Park, CA, USA.
Title:Long-term nicotine treatment down-regulates α6ß2* nicotinic receptor expression and function in nucleus accumbens.
Source:J Neurochem; 127(6):762-71, 2013 Dec.
ISSN:1471-4159
Country of publication:England
Language:eng
Abstract:Long-term nicotine exposure induces alterations in dopamine transmission in nucleus accumbens that sustain the reinforcing effects of smoking. One approach to understand the adaptive changes that arise involves measurement of endogenous dopamine release using voltammetry. We therefore treated rats for 2-3 months with nicotine and examined alterations in nAChR subtype expression and electrically evoked dopamine release in rat nucleus accumbens shell, a region key in addiction. Long-term nicotine treatment selectively decreased stimulated α6ß2* nAChR-mediated dopamine release compared with vehicle-treated rats. It also reduced α6ß2* nAChRs, suggesting the receptor decline may contribute to the functional loss. This decreased response in release after chronic nicotine treatment was still partially sensitive to the agonist nicotine. Studies with an acetylcholinesterase inhibitor demonstrated that the response was also sensitive to increased endogenous acetylcholine. However, unlike the agonists, nAChR antagonists decreased dopamine release only in vehicle- but not nicotine-treated rats. As antagonists function by blocking the action of acetylcholine, their ineffectiveness suggests that reduced acetylcholine levels partly underlie the dampened α6ß2* nAChR-mediated function in nicotine-treated rats. As long-term nicotine modifies dopamine release by decreasing α6ß2* nAChRs and their function, these data suggest that interventions that target this subtype may be useful for treating nicotine dependence. Long-term nicotine treatment decreases dopamine (DA) transmission in the mesolimbic dopaminergic system. Our data suggest this may involve a decrease in α6ß2* nicotinic receptor expression and function. These changes may play a key role in nicotine reward and dependence.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Cholinesterase Inhibitors); 0 (Dopamine Plasma Membrane Transport Proteins); 0 (Nicotinic Agonists); 0 (Nicotinic Antagonists); 0 (Receptors, Nicotinic); 0 (alpha6beta2 nicotinic acetylcholine receptor); 51FOB87G3I (Ambenonium Chloride); 6M3C89ZY6R (Nicotine); VTD58H1Z2X (Dopamine)


  7 / 102 MEDLINE  
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PMID:21397501
Author:Komloova M; Musilek K; Horova A; Holas O; Dohnal V; Gunn-Moore F; Kuca K
Address:Charles University, Faculty of Pharmacy, Department of Pharmaceutical Chemistry and Drug Control, Heyrovskeho 1203, 500 05 Hradec Kralove, Czech Republic.
Title:Preparation, in vitro screening and molecular modelling of symmetrical bis-quinolinium cholinesterase inhibitors--implications for early myasthenia gravis treatment.
Source:Bioorg Med Chem Lett; 21(8):2505-9, 2011 Apr 15.
ISSN:1464-3405
Country of publication:England
Language:eng
Abstract:This paper describes the preparation and in vitro evaluation of 18 newly prepared bis-quinolinium inhibitors on human recombinant acetylcholinesterase (AChE) and human plasmatic butyrylcholinesterase (BChE). Their inhibitory (IC(50)) and was compared to the chosen standards ambenonium dichloride, edrophonium chloride, BW284c51 and ethopropazine hydrochloride. One novel compound was found to be a promising inhibitor of hAChE (in nM range) and was better than edrophonium chloride or BW284c51, but was worse than ambenonium chloride. This compound also showed selectivity towards hAChE and it was confirmed as a non-competitive inhibitor of hAChE by kinetic analysis. A molecular modelling study further confirmed its binding to the peripheral active site of hAChE via apparent π-π or π-cationic interactions.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Name of substance:0 (Cholinesterase Inhibitors); 0 (Quinolinium Compounds); 0 (Recombinant Proteins); 402-40-4 (Benzenaminium, 4,4'-(3-oxo-1,5-pentanediyl)bis(N,N-dimethyl-N-2-propenyl-), Dibromide); 51FOB87G3I (Ambenonium Chloride); 70FP3JLY7N (Edrophonium); EC 3.1.1.7 (Acetylcholinesterase); EC 3.1.1.8 (Butyrylcholinesterase)


  8 / 102 MEDLINE  
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PMID:18340510
Author:Kaneda H; Saito Y; Saito T; Maniwa T; Minami K; Kusaka H; Imamura H
Address:Department of Thoracic and Cardiovascular Surgery, Kansai Medical University Hirakata Hospital, 2-3-1 Shinmachi, Hirakata, Osaka, 573-1191, Japan. kanedah@hirakata.kmu.ac.jp
Title:Preoperative steroid therapy stabilizes postoperative respiratory conditions in myasthenia gravis.
Source:Gen Thorac Cardiovasc Surg; 56(3):114-8, 2008 Mar.
ISSN:1863-6705
Country of publication:Japan
Language:eng
Abstract:OBJECTIVE: We reviewed our experience from 1990 to 2005 to examine whether control of myasthenia gravis (MG) with steroid therapy before surgery could stabilize postoperative respiratory conditions, compared with the nonsteroid treatment. METHODS: Records of 43 consecutive patients with MG who underwent extended thymectomy at Kansai Medical University Hospital were retrospectively reviewed. Two groups, a steroid group (n = 28) and a nonsteroid group (n = 15) were compared. RESULTS: In the steroid group, steroid doses ranged from 10 to 100 mg every other day, or 40-60 mg daily. The patients showed significantly less thymus hyperplasia in the pathological findings (P = 0.023). Whereas 3 of 28 (7%) in the steroid group suffered respiratory insufficiency within 3 days of surgery, 5 of 15 (33%) in the nonsteroid group exhibited the same problem (P = 0.030). Univariate analysis showed that steroid treatment was the only significant factor (P = 0.041) affecting respiratory insufficiency. Patients in the steroid group achieved palliation of MG more quickly after surgery than patients in the nonsteroid group (86% vs. 57% within 6 months, P = 0.059; 84% vs. 42% within 1 year, P = 0.042). CONCLUSION: The control of myasthenia gravis with steroid therapy before surgery seems to stabilize postoperative respiratory status without having adverse effects on surgical infection.
Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE
Name of substance:0 (Cholinesterase Inhibitors); 51FOB87G3I (Ambenonium Chloride); 9PHQ9Y1OLM (Prednisolone)


  9 / 102 MEDLINE  
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PMID:18340506
Author:Fujii Y
Title:Preoperative steroid therapy stabilizes postoperative respiratory condition in myasthenia gravis.
Source:Gen Thorac Cardiovasc Surg; 56(3):95-6, 2008 Mar.
ISSN:1863-6705
Country of publication:Japan
Language:eng
Publication type:COMMENT; EDITORIAL
Name of substance:0 (Cholinesterase Inhibitors); 0 (Glucocorticoids); 51FOB87G3I (Ambenonium Chloride); 9PHQ9Y1OLM (Prednisolone)


  10 / 102 MEDLINE  
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PMID:17464478
Author:Iseki K; Mezaki T; Kawamoto Y; Tomimoto H; Fukuyama H; Shibasaki H
Address:Human Brain Research Center, Kyoto University, 54 Shogoin-Kawaharacho, Sakyo-ku, Kyoto 606-8507, Japan. iseki@kuhp.kyoto-u.ac.jp
Title:Concurrence of non-myasthenic symptoms with myasthenia gravis.
Source:Neurol Sci; 28(2):114-5, 2007 Apr.
ISSN:1590-1874
Country of publication:Italy
Language:eng
Abstract:Myasthenia gravis (MG) is a disease that is known to be accompanied by various complications. But the relationship between these complications and MG and the treatment for these complications still partly remain unknown. We report two cases of MG with unusual complications. The first one is a case of a 72-year-old woman with lingual dyskinesia, and the second is a 28-year-old man with dysgeusia. Both symptoms improved in parallel after the treatment of MG. Here we report these cases and review similar cases in the literature.
Publication type:CASE REPORTS; JOURNAL ARTICLE
Name of substance:51FOB87G3I (Ambenonium Chloride); 9PHQ9Y1OLM (Prednisolone); KVI301NA53 (Pyridostigmine Bromide)



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