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[PMID]:27468972
[Au] Autor:Cozanitis DA
[Ad] Endereço:Department of Anaesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, PO Box 340 (Haartmaninkatu 4), 00029 HUS, Helsinki, Finland. dacozanitis@gmail.com.
[Ti] Título:Daniel Bovet, Nobelist: muscle relaxants in anaesthesia : The role played by two neglected protagonists.
[Ti] Título:Daniel Bovet, Nobelpreisträger: Muskelrelaxanzien in der Anästhesie : Die Rolle zweier vernachlässigter Protagonisten..
[So] Source:Wien Med Wochenschr;166(15-16):487-499, 2016 Nov.
[Is] ISSN:1563-258X
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:In 1957, Professor Daniel Bovet received the Nobel Prize in Physiology or Medicine for his studies on various compounds including the muscle relaxants gallamine and succinylcholine that became very useful in anaesthesia. Textbooks credit Professor Bovet for the discovery of these drugs. However, although he indeed did discover their pharmacological character, the actual syntheses were made by Ernest Fourneau and Reid Hunt, respectively; sadly, these two scientists have largely been ignored. In this paper, a brief biography of Bovet is presented along with some of his more notable accomplishments. Particular emphasis has been placed on gallamine and succinylcholine along with their history. In an attempt to undo the "injustice" dealt to both Fourneau and Hunt, brief accounts of their history, story and character are provided.
[Mh] Termos MeSH primário: Anestesia/história
Trietiodeto de Galamina/história
Fármacos Neuromusculares/história
Prêmio Nobel
Succinilcolina/história
[Mh] Termos MeSH secundário: Animais
França
História do Século XX
Seres Humanos
Suíça
Reino Unido
[Pt] Tipo de publicação:BIOGRAPHY; HISTORICAL ARTICLE; JOURNAL ARTICLE; PORTRAITS
[Ps] Nome de pessoa como assunto:Bovet D; Fourneau E; Hunt R
[Nm] Nome de substância:
0 (Neuromuscular Agents); J2R869A8YF (Succinylcholine); Q3254X40X2 (Gallamine Triethiodide)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160730
[St] Status:MEDLINE


  2 / 1207 MEDLINE  
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[PMID]:25301379
[Au] Autor:de Carvalho MT; Celotto AC; Albuquerque AA; Ferreira LG; Capellini VK; Silveira AP; de Nadai TR; Evora PR
[Ad] Endereço:Department of Surgery and Anatomy, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
[Ti] Título:In vitro effects of the organophosphorus pesticide malathion on the reactivity of rat aorta.
[So] Source:Pharmacology;94(3-4):157-62, 2014.
[Is] ISSN:1423-0313
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: There is a remarkable paucity of studies analyzing the role of the endothelium-derived relaxing factors on the vascular effects of organophosphates. This study was carried out to evaluate the vascular effects of malathion and the role of nitric oxide (NO) and prostacyclin (PGI2). METHODS: Vascular reactivity measuring isometric forces in vitro ('organ chambers') and flow cytometry (cells loaded with DAF-FM DA) were used. RESULTS: In rat thoracic aorta segments contracted with phenylephrine (Phe) (10(-7) mol/l), malathion (10(-10) to 10(-5) mol/l) induced concentration-dependent relaxation in arteries with intact endothelium (n = 7; p < 0.05). Malathion-mediated relaxation was blocked by N-nitro-L-arginine methyl ester (L-NAME; 10(-4) mol/l), a nonspecific NO synthase inhibitor, and/or indomethacin (10(-5) mol/l), a nonspecific cyclooxygenase inhibitor (n = 10, p < 0.05). In thoracic aorta rings, with and without endothelium, Phe (10(-10) to 10(-5) mol/l) evoked concentration-dependent contraction, which was reduced in the presence of malathion. In rings with or without endothelium, incubated with malathion, L-NAME and indomethacin, the Phe-induced contraction was restored. The role of NO was confirmed using flow cytometry. Malathion evokes endothelium-dependent relaxation through the M1 muscarinic receptor, since this relaxation was clearly blocked by atropine (M1 and M2 blocker) and pirenzepine (M1 blocker), but was less blocked by gallamine (M2 blocker) or 4-DAMP (M3 blocker). CONCLUSIONS: These findings suggest that the organophosphate compound effects on vascular reactivity depend of NO and PGI2.
[Mh] Termos MeSH primário: Aorta Torácica/efeitos dos fármacos
Malation/farmacologia
Óxido Nítrico/fisiologia
Praguicidas/farmacologia
Vasodilatadores/farmacologia
[Mh] Termos MeSH secundário: Animais
Aorta Torácica/fisiologia
Atropina/farmacologia
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/fisiologia
Epoprostenol/fisiologia
Trietiodeto de Galamina/farmacologia
Técnicas In Vitro
Indometacina/farmacologia
Masculino
Antagonistas Muscarínicos/farmacologia
NG-Nitroarginina Metil Éster/farmacologia
Óxido Nítrico Sintase/antagonistas & inibidores
Fenilefrina/farmacologia
Piperidinas/farmacologia
Pirenzepina/farmacologia
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Muscarinic Antagonists); 0 (Pesticides); 0 (Piperidines); 0 (Vasodilator Agents); 1WS297W6MV (Phenylephrine); 31C4KY9ESH (Nitric Oxide); 3G0285N20N (Pirenzepine); 7C0697DR9I (Atropine); 81405-11-0 (4-diphenylacetoxy-1,1-dimethylpiperidinium); DCR9Z582X0 (Epoprostenol); EC 1.14.13.39 (Nitric Oxide Synthase); Q3254X40X2 (Gallamine Triethiodide); U5N7SU872W (Malathion); V55S2QJN2X (NG-Nitroarginine Methyl Ester); XXE1CET956 (Indomethacin)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:141118
[Lr] Data última revisão:
141118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141011
[St] Status:MEDLINE
[do] DOI:10.1159/000367897


  3 / 1207 MEDLINE  
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[PMID]:24975101
[Au] Autor:Villamil-Hernández MT; Alcántara-Vázquez O; Sánchez-López A; Gutiérrez-Lara EJ; Centurión D
[Ad] Endereço:Departamento de Farmacobiología, Cinvestav-Coapa, Czda. de los Tenorios 235, Col. Granjas-Coapa, Deleg. Tlalpan, C.P. 14330 México D.F., México.
[Ti] Título:Pharmacological evidence that 5-HT1A/1B/1D, α2-adrenoceptors and D2-like receptors mediate ergotamine-induced inhibition of the vasopressor sympathetic outflow in pithed rats.
[So] Source:Eur J Pharmacol;740:512-21, 2014 Oct 05.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The sympathetic nervous system that innervates the peripheral circulation is regulated by several mechanisms/receptors. It has been reported that prejunctional 5-HT1A, 5-HT1B, 5-HT1D, D2-like receptors and α2-adrenoceptors mediate the inhibition of the vasopressor sympathetic outflow in pithed rats. In addition, ergotamine, an antimigraine drug, displays affinity at the above receptors and may explain some of its adverse/therapeutic effects. Thus, the aims of this study were to investigate in pithed rats: (i) whether ergotamine produces inhibition of the vasopressor sympathetic outflow; and (ii) the major receptors involved in this effect. For this purpose, male Wistar pithed rats were pre-treated with gallamine (25 mg/kg; i.v.) and desipramine (50 µg/kg) and prepared to stimulate the vasopressor sympathetic outflow (T7-T9; 0.03-3 Hz) or to receive i.v. bolus of exogenous noradrenaline (0.03-3 µg/kg). I.v. continuous infusions of ergotamine (1 and 1.8 µg/kgmin) dose-dependently inhibited the vasopressor responses to sympathetic stimulation but not those to exogenous noradrenaline. The sympatho-inhibition elicited by 1.8 µg/kg min ergotamine was (i) unaffected by saline (1 ml/kg); (ii) partially antagonised by WAY 100635 (5-HT1A; 30 µg/kg) and rauwolscine (α2-adrenoceptor; 300 µg/kg), and (iii) dose-dependently blocked by GR 127935 (5-HT1B/1D; 100 and 300 µg/kg) or raclopride (D2-like; 300 and 1000 µg/kg), The above doses of antagonists did not modify per se the sympathetically-induced vasopressor responses. The above results suggest that ergotamine induces inhibition of the vasopressor sympathetic outflow by activation of prejunctional 5-HT1A, 5-HT1B/1D, α2-adrenoceptors and D2-like receptors in pithed rats.
[Mh] Termos MeSH primário: Ergotamina/farmacologia
Receptores Adrenérgicos alfa 2/metabolismo
Receptores de Dopamina D2/metabolismo
Receptores 5-HT1 de Serotonina/metabolismo
[Mh] Termos MeSH secundário: Animais
Pressão Sanguínea/efeitos dos fármacos
Desipramina/farmacologia
Trietiodeto de Galamina/farmacologia
Frequência Cardíaca/efeitos dos fármacos
Masculino
Norepinefrina/farmacologia
Ratos Wistar
Vasoconstritores/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Adrenergic, alpha-2); 0 (Receptors, Dopamine D2); 0 (Receptors, Serotonin, 5-HT1); 0 (Vasoconstrictor Agents); PR834Q503T (Ergotamine); Q3254X40X2 (Gallamine Triethiodide); TG537D343B (Desipramine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:140827
[Lr] Data última revisão:
140827
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140701
[St] Status:MEDLINE


  4 / 1207 MEDLINE  
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[PMID]:23769688
[Au] Autor:Lin JY; Arthurs J; Reilly S
[Ad] Endereço:Department of Psychology, University of Illinois at Chicago, 1007 West Harrison Street, Chicago, IL 60607, United States. jlin2@uic.edu
[Ti] Título:Reduced palatability in pain-induced conditioned taste aversions.
[So] Source:Physiol Behav;119:79-85, 2013 Jul 02.
[Is] ISSN:1873-507X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The current study investigated whether internal pain-inducing agents can modulate palatability of a tastant in the same way as illness-inducing agents (e.g., lithium chloride). Similar to traditional conditioned taste aversion (CTA) experiments, during conditioning the rats were exposed to a saccharin solution followed by intraperitoneal injections of either gallamine (Experiment 1) or hypertonic sodium chloride (NaCl; Experiments 1 and 2). In addition to the total amount consumed, the time of each lick was recorded for lick pattern analysis. The results showed that both gallamine and hypertonic NaCl caused suppression in saccharin intake. Importantly, both lick cluster size and initial lick rate (the measures of taste palatability) were reduced as well. This pattern of results suggests that these pain-inducing agents reduce the hedonic value of the associated tastant and thus CTA is acquired. The current finding serves as evidence supporting the view that CTA is a broadly tuned mechanism that can be triggered by changes in internal body states following consummatory experience.
[Mh] Termos MeSH primário: Aprendizagem da Esquiva
Condicionamento Clássico
Comportamento Alimentar/efeitos dos fármacos
Dor/psicologia
Paladar
[Mh] Termos MeSH secundário: Animais
Aprendizagem da Esquiva/efeitos dos fármacos
Trietiodeto de Galamina/farmacologia
Masculino
Dor/induzido quimicamente
Ratos
Sacarina/farmacologia
Solução Salina Hipertônica/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Saline Solution, Hypertonic); FST467XS7D (Saccharin); Q3254X40X2 (Gallamine Triethiodide)
[Em] Mês de entrada:1404
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130618
[St] Status:MEDLINE


  5 / 1207 MEDLINE  
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[PMID]:23604140
[Au] Autor:Daval SB; Kellenberger E; Bonnet D; Utard V; Galzi JL; Ilien B
[Ad] Endereço:Unité Biotechnologie et Signalisation cellulaire, UMR 7242 CNRS, Université de Strasbourg, Ecole Supérieure de Biotechnologie de Strasbourg, 300 Bvd S. Brant - BP 10413, 67412 Illkirch, France.
[Ti] Título:Exploration of the orthosteric/allosteric interface in human M1 muscarinic receptors by bitopic fluorescent ligands.
[So] Source:Mol Pharmacol;84(1):71-85, 2013 Jul.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bitopic binding properties apply to a variety of muscarinic compounds that span and simultaneously bind to both the orthosteric and allosteric receptor sites. We provide evidence that fluorescent pirenzepine derivatives, with the M1 antagonist fused to the boron-dipyrromethene [Bodipy (558/568)] fluorophore via spacers of varying lengths, exhibit orthosteric/allosteric binding properties at muscarinic M1 receptors. This behavior was inferred from a combination of functional, radioligand, and fluorescence resonance energy transfer binding experiments performed under equilibrium and kinetic conditions on enhanced green fluorescent protein-fused M1 receptors. Although displaying a common orthosteric component, the fluorescent compounds inherit bitopic properties from a linker-guided positioning of their Bodipy moiety within the M1 allosteric vestibule. Depending on linker length, the fluorophore is allowed to reach neighboring allosteric domains, overlapping or not with the classic gallamine site, but distinct from the allosteric indolocarbazole "WIN" site. Site-directed mutagenesis, as well as molecular modeling and ligand docking studies based on recently solved muscarinic receptor structures, further support the definition of two groups of Bodipy-pirenzepine derivatives exhibiting distinct allosteric binding poses. Thus, the linker may dictate pharmacological outcomes for bitopic molecules that are hardly predictable from the properties of individual orthosteric and allosteric building blocks. Our findings also demonstrate that the fusion of a fluorophore to an orthosteric ligand is not neutral, as it may confer, unless carefully controlled, unexpected properties to the resultant fluorescent tracer. Altogether, this study illustrates the importance of a "multifacet" experimental approach to unravel and validate bitopic ligand binding mechanisms.
[Mh] Termos MeSH primário: Compostos de Boro/farmacologia
Corantes Fluorescentes/farmacologia
Pirenzepina/análogos & derivados
Receptor Muscarínico M1/genética
Receptor Muscarínico M1/metabolismo
[Mh] Termos MeSH secundário: Regulação Alostérica
Sítio Alostérico
Cálcio/metabolismo
Linhagem Celular
Linhagem Celular Tumoral
Trietiodeto de Galamina/farmacologia
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Células HEK293
Seres Humanos
Ligantes
Mutagênese Sítio-Dirigida/métodos
Neuroblastoma/genética
Neuroblastoma/metabolismo
Pirenzepina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bodipy-pirenzepine); 0 (Boron Compounds); 0 (Fluorescent Dyes); 0 (Ligands); 0 (Receptor, Muscarinic M1); 0 (enhanced green fluorescent protein); 147336-22-9 (Green Fluorescent Proteins); 3G0285N20N (Pirenzepine); Q3254X40X2 (Gallamine Triethiodide); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1309
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130423
[St] Status:MEDLINE
[do] DOI:10.1124/mol.113.085670


  6 / 1207 MEDLINE  
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[PMID]:23449734
[Au] Autor:Oenema TA; Mensink G; Smedinga L; Halayko AJ; Zaagsma J; Meurs H; Gosens R; Dekkers BG
[Ad] Endereço:Department of Molecular Pharmacology, University of Groningen, Groningen, The Netherlands. t.a.oenema@rug.nl
[Ti] Título:Cross-talk between transforming growth factor-ß1 and muscarinic M2 receptors augments airway smooth muscle proliferation.
[So] Source:Am J Respir Cell Mol Biol;49(1):18-27, 2013 Jul.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transforming growth factor-ß1 (TGF-ß1) is a central mediator in tissue remodeling processes, including fibrosis and airway smooth muscle (ASM) hyperplasia, as observed in asthma. The mechanisms underlying this response, however, remain unclear because TGF-ß1 exerts only weak mitogenic effects on ASM cells. In this study, we hypothesized that the mitogenic effect of TGF-ß1 on ASM is indirect and requires prolonged exposure to allow for extracellular matrix (ECM) deposition. To address this hypothesis, we investigated the effects of acute and prolonged treatment with TGF-ß1, alone and in combination with the muscarinic receptor agonist methacholine, on human ASM cell proliferation. Acutely, TGF-ß1 exerted no mitogenic effect. However, prolonged treatment (for 7 d) with TGF-ß1 increased ASM cell proliferation and potentiated the platelet-derived growth factor-induced mitogenic response. Muscarinic receptor stimulation with methacholine synergistically enhanced the effect of TGF-ß1. Interestingly, the integrin-blocking peptide Arg-Gly-Asp-Ser, as well as integrin α5ß1 function-blocking antibodies, inhibited the effects of TGF-ß1 and its combination with methacholine on cell proliferation. Accordingly, prolonged treatment with TGF-ß1 increased fibronectin expression, which was also synergistically enhanced by methacholine. The synergistic effects of methacholine on TGF-ß1-induced proliferation were reduced by the long-acting muscarinic receptor antagonist tiotropium and the M2 receptor subtype-selective antagonist gallamine, but not the M3-selective antagonist DAU5884. In line with these findings, the irreversible Gi protein inhibitor pertussis toxin also prevented the potentiation of TGF-ß1-induced proliferation by methacholine. We conclude that prolonged exposure to TGF-ß1 enhances ASM cell proliferation, which is mediated by extracellular matrix-integrin interactions, and which can be enhanced by muscarinic M2 receptor stimulation.
[Mh] Termos MeSH primário: Proliferação Celular
Miócitos de Músculo Liso/efeitos dos fármacos
Receptor Cross-Talk
Receptor Muscarínico M2/metabolismo
Fator de Crescimento Transformador beta1/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Transformada
Meios de Cultura Livres de Soro
Replicação do DNA
Sinergismo Farmacológico
Matriz Extracelular/metabolismo
Fibronectinas/metabolismo
Trietiodeto de Galamina/farmacologia
Seres Humanos
Integrina alfa5beta1/metabolismo
Cloreto de Metacolina/farmacologia
Mitógenos/farmacologia
Miócitos de Músculo Liso/metabolismo
Oligopeptídeos/farmacologia
Toxina Pertussis/farmacologia
Receptor Muscarínico M2/agonistas
Sistema Respiratório/citologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Culture Media, Serum-Free); 0 (Fibronectins); 0 (Integrin alpha5beta1); 0 (Mitogens); 0 (Oligopeptides); 0 (Receptor, Muscarinic M2); 0 (Transforming Growth Factor beta1); 0W5ETF9M2K (Methacholine Chloride); AC6UDA2MFC (arginyl-glycyl-aspartyl-serine); EC 2.4.2.31 (Pertussis Toxin); Q3254X40X2 (Gallamine Triethiodide)
[Em] Mês de entrada:1309
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130302
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2012-0261OC


  7 / 1207 MEDLINE  
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[PMID]:23330075
[Au] Autor:Ziyatdinova NI; Sergeeva AM; Dementieva RE; Zefirov TL
[Ad] Endereço:Department of Anatomy, Physiology, and Human Health Protection, Kazan (Volga Region) Federal University, Russia.
[Ti] Título:Peculiar effects of muscarinic M1, M2, and M3 receptor blockers on cardiac chronotropic function in neonatal rats.
[So] Source:Bull Exp Biol Med;154(1):1-2, 2012 Nov.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng; rus
[Ab] Resumo:The effects of muscarinic M(1), M(2), and M(3) cholinergic receptor blockade on the regulation of chronotropic function of the heart were studied in vivo in 7-day-old rat pups. Intravenous injection of M(2) receptor blocker gallamine produced no changes in cardiac chronotropy. In contrast, M(1) receptor blocker pirenzepine and M(3) receptor blocker 4DAMP provoked bradycardia. These data attest to the involvement of M(1) and especially M(3) cholinergic receptors in the regulation of cardiac chronotropy in rat pups, which confirms the view on pronounced species-specific and age-related peculiarities in the heart control mechanisms.
[Mh] Termos MeSH primário: Frequência Cardíaca/efeitos dos fármacos
Frequência Cardíaca/fisiologia
Antagonistas Muscarínicos/farmacologia
Receptor Muscarínico M1/antagonistas & inibidores
Receptor Muscarínico M2/antagonistas & inibidores
Receptor Muscarínico M3/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Trietiodeto de Galamina/farmacologia
Piperidinas/farmacologia
Pirenzepina/farmacologia
Ratos
Estimulação Química
Nervo Vago/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Muscarinic Antagonists); 0 (Piperidines); 0 (Receptor, Muscarinic M1); 0 (Receptor, Muscarinic M2); 0 (Receptor, Muscarinic M3); 3G0285N20N (Pirenzepine); 81405-11-0 (4-diphenylacetoxy-1,1-dimethylpiperidinium); Q3254X40X2 (Gallamine Triethiodide)
[Em] Mês de entrada:1305
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130119
[St] Status:MEDLINE


  8 / 1207 MEDLINE  
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[PMID]:22551249
[Au] Autor:Shivnaraine RV; Huang XP; Seidenberg M; Ellis J; Wells JW
[Ad] Endereço:Department of Pharmaceutical Sciences, University of Toronto, Toronto, Ontario, Canada M5S 3M2.
[Ti] Título:Heterotropic cooperativity within and between protomers of an oligomeric M(2) muscarinic receptor.
[So] Source:Biochemistry;51(22):4518-40, 2012 Jun 05.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:At least four allosteric sites have been found to mediate the dose-dependent effects of gallamine on the binding of [(3)H]quinuclidinylbenzilate (QNB) and N-[(3)H]methylscopolamine (NMS) to M(2) muscarinic receptors in membranes and solubilized preparations from porcine atria, CHO cells, and Sf9 cells. The rate of dissociation of [(3)H]QNB was affected in a bell-shaped manner with at least one Hill coefficient (n(H)) greater than 1, indicating that at least three allosteric sites are involved. The level of binding of [(3)H]QNB was decreased in a biphasic manner, revealing at least two allosteric sites; binding of [(3)H]NMS was affected in a triphasic, serpentine manner, revealing at least three sites, and values of n(H) >1 pointed to at least four sites. Several lines of evidence indicate that all effects of gallamine were allosteric in nature and could be observed at equilibrium. The rates of equilibration and dissociation suggest that the receptor was predominately oligomeric, and the heterogeneity revealed by gallamine can be attributed to differences in its affinity for the constituent protomers of a tetramer. Those differences appear to arise from inter- and intramolecular cooperativity between gallamine and the radioligand.
[Mh] Termos MeSH primário: Antagonistas Colinérgicos/farmacologia
Trietiodeto de Galamina/farmacologia
N-Metilescopolamina/farmacologia
Subunidades Proteicas/metabolismo
Quinuclidinil Benzilato/farmacologia
Receptor Muscarínico M2/metabolismo
[Mh] Termos MeSH secundário: Regulação Alostérica/efeitos dos fármacos
Sítio Alostérico
Animais
Células CHO
Cricetinae
Cinética
Antagonistas Muscarínicos/farmacologia
Subunidades Proteicas/antagonistas & inibidores
Subunidades Proteicas/química
Receptor Muscarínico M2/antagonistas & inibidores
Receptor Muscarínico M2/química
Células Sf9
Solubilidade
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cholinergic Antagonists); 0 (Muscarinic Antagonists); 0 (Protein Subunits); 0 (Receptor, Muscarinic M2); 6581-06-2 (Quinuclidinyl Benzilate); Q3254X40X2 (Gallamine Triethiodide); VDR09VTQ8U (N-Methylscopolamine)
[Em] Mês de entrada:1212
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120504
[St] Status:MEDLINE


  9 / 1207 MEDLINE  
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[PMID]:22490561
[Au] Autor:Zheng F; Wess J; Alzheimer C
[Ad] Endereço:Institute of Physiology, University of Kiel, Kiel, Germany.
[Ti] Título:M2 muscarinic acetylcholine receptors regulate long-term potentiation at hippocampal CA3 pyramidal cell synapses in an input-specific fashion.
[So] Source:J Neurophysiol;108(1):91-100, 2012 Jul.
[Is] ISSN:1522-1598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Muscarinic receptors have long been known as crucial players in hippocampus-dependent learning and memory, but our understanding of the cellular underpinnings and the receptor subtypes involved lags well behind. This holds in particular for the hippocampal CA3 region, where the mechanisms of synaptic plasticity depend on the type of afferent input. Williams and Johnston (Williams S, Johnston D. Science 242: 84-87, 1988; Williams S, Johnston D. J Neurophysiol 64: 1089-1097, 1990) demonstrated muscarinic depression of mossy fiber (MF) long-term potentiation (LTP) through a presynaptic site of action and Maeda et al. (Maeda T, Kaneko S, Satoh M. Brain Res 619: 324-330, 1993) proposed a bidirectional modulation of MF LTP by muscarinic receptor subtypes. Since then, this issue, as well as muscarinic regulation of plasticity at associational/commissural (A/C) fiber-CA3 synapses has remained largely neglected, not least because of the lack of highly selective ligands for the different muscarinic receptor subtypes. In the present study, we performed field potential and whole cell recordings from the hippocampal CA3 region of M(2) receptor knockout mice to determine the role of M(2) receptors in short-term and long-term plasticity at A/C and MF inputs to CA3 pyramidal cells. At the A/C synapse, M(2) receptors promoted short-term facilitation and LTP. Unexpectedly, M(2) receptors mediated the opposite effect on LTP at the MF synapse, which was significantly reduced, most likely involving a depressant effect of M(2) receptors on adenylyl cyclase activity in MF terminals. Our data demonstrate that cholinergic projections recruit M(2) receptors to redistribute the gain of LTP in CA3 pyramidal cells in an input-specific manner.
[Mh] Termos MeSH primário: Região CA3 Hipocampal/citologia
Potenciação de Longa Duração/fisiologia
Células Piramidais/fisiologia
Receptor Muscarínico M2/metabolismo
Sinapses/fisiologia
[Mh] Termos MeSH secundário: Animais
Antracenos/farmacologia
Anticonvulsivantes/farmacologia
Fenômenos Biofísicos/efeitos dos fármacos
Fenômenos Biofísicos/genética
Bungarotoxinas/farmacologia
Colforsina/farmacologia
Ciclopropanos/farmacologia
Estimulação Elétrica
Inibidores Enzimáticos/farmacologia
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Potenciais Pós-Sinápticos Excitadores/genética
Antagonistas GABAérgicos/farmacologia
Trietiodeto de Galamina/farmacologia
Glicina/análogos & derivados
Glicina/farmacologia
Técnicas In Vitro
Potenciação de Longa Duração/efeitos dos fármacos
Potenciação de Longa Duração/genética
Camundongos
Camundongos Knockout
Rede Nervosa/fisiologia
Antagonistas Nicotínicos/farmacologia
Técnicas de Patch-Clamp
Ácidos Fosfínicos/farmacologia
Propanolaminas/farmacologia
Receptor Muscarínico M2/deficiência
Sinapses/efeitos dos fármacos
Sinapses/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (2,3-didecyloxyanthracene); 0 (Anthracenes); 0 (Anticonvulsants); 0 (Bungarotoxins); 0 (Cyclopropanes); 0 (Enzyme Inhibitors); 0 (GABA Antagonists); 0 (Nicotinic Antagonists); 0 (Phosphinic Acids); 0 (Propanolamines); 0 (Receptor, Muscarinic M2); 147782-19-2 (2-(2,3-dicarboxycyclopropyl)glycine); 148056-42-2 (CGP 55845A); 1F7A44V6OU (Colforsin); Q3254X40X2 (Gallamine Triethiodide); TE7660XO1C (Glycine)
[Em] Mês de entrada:1211
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120412
[St] Status:MEDLINE
[do] DOI:10.1152/jn.00740.2011


  10 / 1207 MEDLINE  
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[PMID]:21966790
[Au] Autor:Lima-Morales I
[Ti] Título:[Intravenous procaine as analgesic in obstetrics. 1955].
[Ti] Título:La procaína endovenosa como analgésico en obstetricia. Julio-Agosto 1955..
[So] Source:Ginecol Obstet Mex;79(2):97-104, 2011 Feb.
[Is] ISSN:0300-9041
[Cp] País de publicação:Mexico
[La] Idioma:spa
[Mh] Termos MeSH primário: Analgesia Obstétrica/história
Anestésicos Locais/história
Obstetrícia/história
Procaína/história
[Mh] Termos MeSH secundário: Anestésicos Locais/administração & dosagem
Anestésicos Locais/farmacologia
Feminino
Feto/efeitos dos fármacos
Trietiodeto de Galamina/administração & dosagem
Trietiodeto de Galamina/história
História do Século XX
Seres Humanos
Recém-Nascido
Injeções Intravenosas
México
Gravidez
Procaína/administração & dosagem
Procaína/farmacologia
[Pt] Tipo de publicação:BIOGRAPHY; CLASSICAL ARTICLE; HISTORICAL ARTICLE; JOURNAL ARTICLE
[Ps] Nome de pessoa como assunto:Lima-Morales I
[Nm] Nome de substância:
0 (Anesthetics, Local); 4Z8Y51M438 (Procaine); Q3254X40X2 (Gallamine Triethiodide)
[Em] Mês de entrada:1111
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111005
[St] Status:MEDLINE



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