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[PMID]:28712745
[Au] Autor:Franks CE; Campbell ST; Purow BW; Harris TE; Hsu KL
[Ad] Endereço:Department of Chemistry, University of Virginia, Charlottesville, VA 22904, USA.
[Ti] Título:The Ligand Binding Landscape of Diacylglycerol Kinases.
[So] Source:Cell Chem Biol;24(7):870-880.e5, 2017 Jul 20.
[Is] ISSN:2451-9456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diacylglycerol kinases (DGKs) are integral components of signal transduction cascades that regulate cell biology through ATP-dependent phosphorylation of the lipid messenger diacylglycerol. Methods for direct evaluation of DGK activity in native biological systems are lacking and needed to study isoform-specific functions of these multidomain lipid kinases. Here, we utilize ATP acyl phosphate activity-based probes and quantitative mass spectrometry to define, for the first time, ATP and small-molecule binding motifs of representative members from all five DGK subtypes. We use chemical proteomics to discover an unusual binding mode for the DGKα inhibitor, ritanserin, including interactions at the atypical C1 domain distinct from the ATP binding region. Unexpectedly, deconstruction of ritanserin yielded a fragment compound that blocks DGKα activity through a conserved binding mode and enhanced selectivity against the kinome. Collectively, our studies illustrate the power of chemical proteomics to profile protein-small molecule interactions of lipid kinases for fragment-based lead discovery.
[Mh] Termos MeSH primário: Diacilglicerol Quinase/metabolismo
Ligantes
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/química
Trifosfato de Adenosina/metabolismo
Sítios de Ligação
Cromatografia Líquida de Alta Pressão
Diacilglicerol Quinase/química
Diacilglicerol Quinase/genética
Células HEK293
Seres Humanos
Marcação por Isótopo
Ketanserina/química
Ketanserina/metabolismo
Peptídeos/análise
Ligação Proteica
Isoformas de Proteínas/química
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Proteoma/análise
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/química
Proteínas Recombinantes/isolamento & purificação
Ritanserina/química
Ritanserina/metabolismo
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ligands); 0 (Peptides); 0 (Protein Isoforms); 0 (Proteome); 0 (Recombinant Proteins); 145TFV465S (Ritanserin); 8L70Q75FXE (Adenosine Triphosphate); 97F9DE4CT4 (Ketanserin); EC 2.7.1.107 (Diacylglycerol Kinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE


  2 / 2896 MEDLINE  
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[PMID]:28233634
[Au] Autor:Sasaki-Hamada S; Suzuki A; Ueda Y; Matsumoto K; Oka JI
[Ad] Endereço:Laboratory of Pharmacology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Japan.
[Ti] Título:Serotonergic and dopaminergic systems are implicated in antidepressant-like effects of chotosan, a Kampo formula, in mice.
[So] Source:J Pharmacol Sci;133(2):110-113, 2017 Feb.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:We previously demonstrated that chotosan (CTS), a traditional herbal formula called Kampo medicine, improves diabetes-induced cognitive deficits. In the present study, we investigated the antidepressant-like effects of CTS in mice. The administration of CTS (1.0 g/kg, for 3 days) decreased the immobility time in the forced-swim test, and this decrease was prevented by the prior administration of sulpiride (an antagonist of D receptors) and WAY100635 (an antagonist of 5-HT receptors). None of the treatments tested altered the locomotor activity of mice. These results suggest that CTS exerts antidepressant-like effects through changes in the serotonergic and dopaminergic systems.
[Mh] Termos MeSH primário: Antidepressivos/farmacologia
Dopaminérgicos/farmacologia
Medicamentos de Ervas Chinesas/farmacologia
Medicina Kampo
Serotoninérgicos/farmacologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Fenclonina/química
Imipramina/química
Imipramina/farmacologia
Ketanserina/química
Ketanserina/farmacologia
Locomoção
Masculino
Metergolina/química
Camundongos
Piperazinas/química
Piperazinas/farmacologia
Piridinas/química
Piridinas/farmacologia
Sulpirida/química
Sulpirida/farmacologia
Natação
Ioimbina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents); 0 (Dopamine Agents); 0 (Drugs, Chinese Herbal); 0 (Piperazines); 0 (Pyridines); 0 (Serotonin Agents); 0 (choto-san); 1501393LY5 (Metergoline); 2Y49VWD90Q (Yohimbine); 71IH826FEG (N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide); 7MNE9M8287 (Sulpiride); 97F9DE4CT4 (Ketanserin); OGG85SX4E4 (Imipramine); R5J7E3L9SP (Fenclonine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE


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[PMID]:27918061
[Au] Autor:Grasso C; Li Volsi G; Barresi M
[Ad] Endereço:Department of Bio-medical Sciences, Section of Physiology, University of Catania, Viale Andrea Doria 6, I-95125 Catania, Italy - Email: clgrasso@unict.it.
[Ti] Título:Serotonin modifies the spontaneous spiking activity of gracile nucleus neurons in rats: role of 5-HT1A and 5-HT2 receptors.
[So] Source:Arch Ital Biol;154(2-3):39-49, 2016 Jun 01.
[Is] ISSN:0003-9829
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:We tested the effects of microiontophoretic application of serotonin (5-HT) on the firing rate of neurons located in the gracile nucleus (GN) of rats. Application of 5-HT1A and 5-HT2 agonists and antagonists respectively mimicked/ modulated and blocked the effects produced by the amine, respectively. Among the tested neurons, 88.2% modified their background firing activity in the presence of 5-HT. Responsive neurons decreased their mean firing activity (MFA) in 56.7% of cases and increased it in the remaining 43.3%. To ascertain the specificity of the effects induced by 5-HT, we utilized 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) and alpha-methyl-5-hydroxytryptamine (α-MET-5-HT), agonists for 5-HT1A and 5-HT2 receptors, respectively. The microiontophoresis of 8-OH-DPAT modified the background firing rate of all GN neurons (100% of tested neurons) mimicking the decrease of MFA evoked by 5-HT. The application of a-MET-5-HT modified the MFA in 76.9% of tested neurons, decreasing it in 61.5% of cases and increasing in the remaining 23.1%. The decrease of MFA induced by 8-OH-DPAT was antagonized by application of the 5-HT1A receptor antagonist N-[2-[-(2-Methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide maleate salt (WAY100635), while application of 5-HT2 receptor antagonist ketanserine tartrate (KET) antagonized only the increase of MFA induced by a-MET-5-HT. These results indicate that 5-HT is able to modulate the background firing activity of GN neurons by 5-HT1A and 5-HT2 receptors.
[Mh] Termos MeSH primário: Potenciais de Ação/efeitos dos fármacos
Bulbo/citologia
Neurônios/efeitos dos fármacos
Serotonina/farmacologia
[Mh] Termos MeSH secundário: 8-Hidroxi-2-(di-n-propilamino)tetralina/farmacologia
Animais
Iontoforese
Ketanserina/farmacologia
Masculino
Piperazinas/farmacologia
Piridinas/farmacologia
Ratos
Ratos Wistar
Receptor 5-HT1A de Serotonina
Receptores 5-HT2 de Serotonina
Serotonina/análogos & derivados
Agonistas de Receptores 5-HT1 de Serotonina/farmacologia
Antagonistas do Receptor 5-HT1 de Serotonina/farmacologia
Agonistas de Receptores 5-HT2 de Serotonina/farmacologia
Antagonistas do Receptor 5-HT2 de Serotonina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Piperazines); 0 (Pyridines); 0 (Receptors, Serotonin, 5-HT2); 0 (Serotonin 5-HT1 Receptor Agonists); 0 (Serotonin 5-HT1 Receptor Antagonists); 0 (Serotonin 5-HT2 Receptor Agonists); 0 (Serotonin 5-HT2 Receptor Antagonists); 112692-38-3 (Receptor, Serotonin, 5-HT1A); 22965-81-7 (alpha-methylserotonin); 333DO1RDJY (Serotonin); 71IH826FEG (N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide); 78950-78-4 (8-Hydroxy-2-(di-n-propylamino)tetralin); 97F9DE4CT4 (Ketanserin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170315
[Lr] Data última revisão:
170315
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161206
[St] Status:MEDLINE
[do] DOI:10.4449/aib.v154i2/3.3430


  4 / 2896 MEDLINE  
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[PMID]:27568460
[Au] Autor:Chen L; Liu DH; Zhang X; Zhang EH; Liu C; Su DF; Cai GJ
[Ad] Endereço:Department of Pharmacology, School of Pharmacy, Second Military Medical University, 325 Guo He Road, Shanghai, China.
[Ti] Título:Baroreflex deficiency aggravates atherosclerosis via α7 nicotinic acetylcholine receptor in mice.
[So] Source:Vascul Pharmacol;87:92-99, 2016 Dec.
[Is] ISSN:1879-3649
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Inflammation and oxidative stress play a key role in the initiation, propagation, and development of atherosclerosis. Arterial baroreflex (ABR) dysfunction induced by sinoaortic denervation (SAD) promoted the development of atherosclerosis in ApoE mice. The present work was designed to examine whether ABR deficiency affected inflammation and oxidative stress via α7 nicotinic acetylcholine receptor (α7nAChR) leading to the aggravation of atherosclerosis in mice. METHODS AND RESULTS: ApoE mice were fed with a high-cholesterol diet for 6weeks and half of the mice received sinoaortic denervation that destroyed ABR. We studied the expression of vesicular acetylcholine transporter (VAChT), α7nAChR and levels of inflammatory response and oxidative stress. The results showed that baroreflex dysfunction could promote atherosclerosis, meanwhile, decrease the expression of VAChT and α7nAChR and significantly increase the levels of oxidative stress and inflammation in SAD mice. After treated with PNU-282987 (a selective α7nAChR agonist, 0.53mg/kg/day) for 6weeks in SAD and Sham mice, we found that PNU-282987 could attenuate atherosclerosis and significantly decreased oxidative stress and inflammation after SAD. In addition, α7nAChR and α7nAChR mice fed with a high-cholesterol diet for 8weeks were co-treated with ketanserin (0.6mg/kg/day), a drug that can enhance baroreflex sensitivity (BRS). Ketanserin could alleviate atherosclerosis and markedly decrease oxidative stress and inflammation in α7nAChR mice. But there were no effects in α7nAChR knockout mice. CONCLUSIONS: Our results demonstrate that ABR dysfunction aggravates atherosclerosis in mice via the vagus-ACh-α7nAChR-inflammation and oxidative stress pathway.
[Mh] Termos MeSH primário: Aterosclerose/patologia
Barorreflexo/fisiologia
Inflamação/patologia
Receptor Nicotínico de Acetilcolina alfa7/metabolismo
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas E/genética
Artérias/fisiologia
Benzamidas/farmacologia
Compostos Bicíclicos com Pontes/farmacologia
Modelos Animais de Doenças
Ketanserina/farmacologia
Camundongos
Camundongos Knockout
Estresse Oxidativo/fisiologia
Receptor Nicotínico de Acetilcolina alfa7/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Benzamides); 0 (Bridged Bicyclo Compounds); 0 (PNU-282987); 0 (alpha7 Nicotinic Acetylcholine Receptor); 97F9DE4CT4 (Ketanserin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160829
[St] Status:MEDLINE


  5 / 2896 MEDLINE  
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[PMID]:27385190
[Au] Autor:Younkin J; Gaitonde SA; Ellaithy A; Vekariya R; Baki L; Moreno JL; Shah S; Drossopoulos P; Hideshima KS; Eltit JM; González-Maeso J; Logothetis DE; Dukat M; Glennon RA
[Ad] Endereço:Department of Physiology and Biophysics, School of Medicine, and ‡Department of Medicinal Chemistry, School of Pharmacy, Virginia Commonwealth University , Richmond, Virginia 23298, United States.
[Ti] Título:Reformulating a Pharmacophore for 5-HT2A Serotonin Receptor Antagonists.
[So] Source:ACS Chem Neurosci;7(9):1292-9, 2016 Sep 21.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Several pharmacophore models have been proposed for 5-HT2A serotonin receptor antagonists. These typically consist of two aromatic/hydrophobic moieties separated by a given distance from each other, and from a basic amine. Although specified distances might vary, the models are relatively similar in their general construction. Because our preliminary data indicated that two aromatic (hydrophobic) moieties might not be required for such action, we deconstructed the serotonin-dopamine antipsychotic agent risperidone (1) into four smaller structural fragments that were thoroughly examined in 5-HT2A receptor binding and functional (i.e., two-electrode voltage clamp (TEVC) and intracellular calcium release) assays. It was apparent that truncated risperidone analogues behaved as antagonists. In particular, 6-fluoro-3-(1-methylpiperidin-4-yl)benzisoxazole (4) displayed high affinity for 5-HT2A receptors (Ki of ca. 12 nM) relative to risperidone (Ki of ca. 5 nM) and behaved as a potent 5-HT2A serotonin receptor antagonist. These results suggest that multiple aromatic (hydrophobic) moieties are not essential for high-affinity 5-HT2A receptor binding and antagonist activity and that current pharmacophore models for such agents are very much in need of revision.
[Mh] Termos MeSH primário: Potenciais da Membrana/efeitos dos fármacos
Antagonistas do Receptor 5-HT2 de Serotonina/síntese química
Antagonistas do Receptor 5-HT2 de Serotonina/farmacologia
[Mh] Termos MeSH secundário: Animais
Bário/farmacologia
Cálcio/metabolismo
Canais de Potássio Corretores do Fluxo de Internalização Acoplados a Proteínas G/genética
Canais de Potássio Corretores do Fluxo de Internalização Acoplados a Proteínas G/metabolismo
Células HEK293
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas/efeitos dos fármacos
Ketanserina/farmacocinética
Ketanserina/farmacologia
Potenciais da Membrana/genética
Mutação/genética
Oócitos
Ligação Proteica/efeitos dos fármacos
Receptor 5-HT2A de Serotonina/genética
Receptor 5-HT2A de Serotonina/metabolismo
Risperidona/farmacologia
Serotonina/farmacologia
Antagonistas do Receptor 5-HT2 de Serotonina/química
Antagonistas da Serotonina/farmacocinética
Antagonistas da Serotonina/farmacologia
Trítio/farmacocinética
Xenopus laevis
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (G Protein-Coupled Inwardly-Rectifying Potassium Channels); 0 (Receptor, Serotonin, 5-HT2A); 0 (Serotonin 5-HT2 Receptor Antagonists); 0 (Serotonin Antagonists); 10028-17-8 (Tritium); 24GP945V5T (Barium); 333DO1RDJY (Serotonin); 97F9DE4CT4 (Ketanserin); L6UH7ZF8HC (Risperidone); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160708
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.6b00162


  6 / 2896 MEDLINE  
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[PMID]:27264435
[Au] Autor:Schenk S; Foote J; Aronsen D; Bukholt N; Highgate Q; Van de Wetering R; Webster J
[Ad] Endereço:School of Psychology, Victoria University of Wellington, Wellington, New Zealand. Electronic address: susan.schenk@vuw.ac.nz.
[Ti] Título:Serotonin antagonists fail to alter MDMA self-administration in rats.
[So] Source:Pharmacol Biochem Behav;148:38-45, 2016 Sep.
[Is] ISSN:1873-5177
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute exposure to ±3,4-methylenedioxymethamphetamine (MDMA) preferentially increases release of serotonin (5-HT), and a role of 5-HT in many of the behavioral effects of acute exposure to MDMA has been demonstrated. A role of 5-HT in MDMA self-administration in rats has not, however, been adequately determined. Therefore, the present study measured the effect of pharmacological manipulation of some 5-HT receptor subtypes on self-administration of MDMA. Rats received extensive experience with self-administered MDMA prior to tests with 5-HT ligands. Doses of the 5-HT1A antagonist, WAY 100635 (0.1-1.0mg/kg), 5-HT1B antagonist, GR 127935 (1.0-3.0mg/kg), and the 5-HT2A antagonist, ketanserin (1.0-3.0mg/kg) that have previously been shown to decrease self-administration of other psychostimulants and that decreased MDMA-produced hyperactivity in the present study did not alter MDMA self-administration. Experimenter-administered injections of MDMA (10.0mg/kg, ip) reinstated extinguished drug-taking behavior, but this also was not decreased by any of the antagonists. In contrast, both WAY 100635 and ketanserin, but not GR 127935, decreased cocaine-produced drug seeking in rats that had been trained to self-administered cocaine. The 5-HT1A agonist, 8-OH-DPAT (0.1-1.0mg/kg), but not the 5-HT1B/1A agonist, RU 24969 (0.3-3.0mg/kg), decreased drug-seeking produced by the reintroduction of a light stimulus that had been paired with self-administered MDMA infusions. These findings suggest a limited role of activation of 5-HT1A, 5-HT1B or 5-HT2 receptor mechanisms in MDMA self-administration or in MDMA-produced drug-seeking following extinction. The data suggest, however, that 5-HT1A agonists inhibit cue-induced drug-seeking following extinction of MDMA self-administration and might, therefore, be useful adjuncts to therapies to limit relapse to MDMA use.
[Mh] Termos MeSH primário: N-Metil-3,4-Metilenodioxianfetamina/administração & dosagem
Autoadministração
Antagonistas da Serotonina/farmacologia
[Mh] Termos MeSH secundário: 8-Hidroxi-2-(di-n-propilamino)tetralina/farmacologia
Animais
Comportamento de Procura de Droga/efeitos dos fármacos
Extinção Psicológica
Ketanserina/farmacologia
Masculino
Oxidiazóis/farmacologia
Piperazinas/farmacologia
Piridinas/farmacologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oxadiazoles); 0 (Piperazines); 0 (Pyridines); 0 (Serotonin Antagonists); 2LLH6CEB40 (GR 127935); 71IH826FEG (N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide); 78950-78-4 (8-Hydroxy-2-(di-n-propylamino)tetralin); 97F9DE4CT4 (Ketanserin); KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160607
[St] Status:MEDLINE


  7 / 2896 MEDLINE  
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[PMID]:27150816
[Au] Autor:de Paula BB; Leite-Panissi CR
[Ad] Endereço:Psychobiology Graduate Program, University of São Paulo - Ribeirão Preto Dentistry School - Dept. Morphology, Physiology and Basic Pathology 14040-901, SP, Brazil.
[Ti] Título:Distinct effect of 5-HT1A and 5-HT2A receptors in the medial nucleus of the amygdala on tonic immobility behavior.
[So] Source:Brain Res;1643:152-8, 2016 Jul 15.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The tonic immobility (TI) response is an innate fear behavior associated with intensely dangerous situations, exhibited by many species of invertebrate and vertebrate animals. In humans, it is possible that TI predicts the severity of posttraumatic stress disorder symptoms. This behavioral response is initiated and sustained by the stimulation of various groups of neurons distributed in the telencephalon, diencephalon and brainstem. Previous research has found the highest Fos-IR in the posteroventral part of the medial nucleus of the amygdala (MEA) during TI behavior; however, the neurotransmission of this amygdaloid region involved in the modulation of this innate fear behavior still needs to be clarified. Considering that a major drug class used for the treatment of psychopathology is based on serotonin (5-HT) neurotransmission, we investigated the effects of serotonergic receptor activation in the MEA on the duration of TI. The results indicate that the activation of the 5HT1A receptors or the blocking of the 5HT2 receptors of the MEA can promote a reduction in fear and/or anxiety, consequently decreasing TI duration in guinea pigs. In contrast, blocking the 5HT1A receptors or activating the 5HT2 receptors in this amygdalar region increased the TI duration, suggesting an increase in fear and/or anxiety. These alterations do not appear to be due to a modification of spontaneous motor activity, which might non-specifically affect TI duration. Thus, these results suggest a distinct role of the 5HT receptors in the MEA in innate fear modulation.
[Mh] Termos MeSH primário: Complexo Nuclear Corticomedial/fisiologia
Medo/fisiologia
Resposta de Imobilidade Tônica
Receptor 5-HT1A de Serotonina/fisiologia
Receptor 5-HT2A de Serotonina/fisiologia
[Mh] Termos MeSH secundário: 8-Hidroxi-2-(di-n-propilamino)tetralina/administração & dosagem
Animais
Ansiedade/fisiopatologia
Complexo Nuclear Corticomedial/efeitos dos fármacos
Medo/efeitos dos fármacos
Cobaias
Resposta de Imobilidade Tônica/efeitos dos fármacos
Ketanserina/administração & dosagem
Masculino
Agonistas de Receptores 5-HT1 de Serotonina/administração & dosagem
Antagonistas do Receptor 5-HT2 de Serotonina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, Serotonin, 5-HT2A); 0 (Serotonin 5-HT1 Receptor Agonists); 0 (Serotonin 5-HT2 Receptor Antagonists); 112692-38-3 (Receptor, Serotonin, 5-HT1A); 78950-78-4 (8-Hydroxy-2-(di-n-propylamino)tetralin); 97F9DE4CT4 (Ketanserin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160507
[St] Status:MEDLINE


  8 / 2896 MEDLINE  
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[PMID]:27079619
[Au] Autor:Silva S; Carvalho F; Fernandes E; Antunes MJ; Cotrim MD
[Ad] Endereço:Group of Pharmacology and Pharmaceutical Care, Faculty of Pharmacy, University of Coimbra, Portugal. Electronic address: sonias@ci.uc.pt.
[Ti] Título:Contractile effects of 3,4-methylenedioxymethamphetamine on the human internal mammary artery.
[So] Source:Toxicol In Vitro;34:187-93, 2016 Aug.
[Is] ISSN:1879-3177
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Since the late 1980s numerous reports have detailed adverse reactions to the use of 3,4-methylenedioxymethamphetamine (MDMA) associated with cardiovascular collapse and sudden death, following ventricular tachycardia and hypertension. For a better understanding of the effects of MDMA on the cardiovascular system, it is critical to determine their effects at the vasculature level, including the transporter or neurotransmitter systems that are most affected at the whole range of drug doses. With this purpose in mind, the aim of our study was to evaluate the contractile effect of MDMA in the human internal mammary artery, the contribution of SERT for this effect and the responsiveness of this artery to 5-HT in the presence of MDMA. We have also studied the possible involvement of 5-HT2 receptors on the MDMA contractile effect in this human blood vessel using ketanserin. Our results showed that MDMA contracted the studied human's internal mammary artery in a SERT-independent form, through activation of 5-HT2A receptors. Considering the high plasma concentrations achieved in heavy users or in situations of acute exposure to drugs, this effect is probably involved in the cardiovascular risk profile of this psychostimulant, especially in subjects with pre-existing cardiovascular disease.
[Mh] Termos MeSH primário: Alucinógenos/farmacologia
Artéria Torácica Interna/efeitos dos fármacos
N-Metil-3,4-Metilenodioxianfetamina/farmacologia
Receptor 5-HT2A de Serotonina/fisiologia
[Mh] Termos MeSH secundário: Fluoxetina/farmacologia
Seres Humanos
Técnicas In Vitro
Contração Isométrica/efeitos dos fármacos
Ketanserina/farmacologia
Artéria Torácica Interna/fisiologia
Receptor 5-HT2C de Serotonina/fisiologia
Serotonina/farmacologia
Antagonistas da Serotonina/farmacologia
Proteínas da Membrana Plasmática de Transporte de Serotonina/fisiologia
Inibidores da Captação de Serotonina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hallucinogens); 0 (Receptor, Serotonin, 5-HT2A); 0 (Receptor, Serotonin, 5-HT2C); 0 (SLC6A4 protein, human); 0 (Serotonin Antagonists); 0 (Serotonin Plasma Membrane Transport Proteins); 0 (Serotonin Uptake Inhibitors); 01K63SUP8D (Fluoxetine); 333DO1RDJY (Serotonin); 97F9DE4CT4 (Ketanserin); KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170323
[Lr] Data última revisão:
170323
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160416
[St] Status:MEDLINE


  9 / 2896 MEDLINE  
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[PMID]:27040714
[Au] Autor:Hu W; Zhang Y; Cai Q; Wang D; Hong Y
[Ad] Endereço:College of Life Sciences, Fujian Normal University, People's Republic of China.
[Ti] Título:Blockade of 5-HT2A receptors at the site of inflammation inhibits activation of spinal dorsal horn neurons in rats.
[So] Source:Brain Res Bull;124:85-94, 2016 Jun.
[Is] ISSN:1873-2747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Repeated inflammation in the periphery is a major cause of chronic inflammatory pain. We have showed that blockade of 5-HT2A receptors in the periphery inhibits repeated inflammation-induced pain hypersensitivity. The present study investigated whether inhibition of 5-HT2A receptor signaling at the site of inflammation could inhibit repeated inflammation-induced neurochemical changes in spinal dorsal horn neurons. Treatment with the 5-HT2A receptor antagonist ketanserin (20µg) in the hindpaw following intraplantar injection of carrageenan inhibited the increase in nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity, a marker of nitric oxide synthase (NOS), in the spinal dorsal horn. Administration of formalin (1%) in the hindpaw following the carrageenan injection evoked a great increase in NADPH-d reactivity in spinal dorsal horn neurons on the ipsilateral and contralateral sides. These changes were abolished by the pretreatment of ketanserin (20µg). The ketanserin treatment also reduced the repeated inflammation-induced expression of protein kinase gamma (PKCγ) in the membrane of spinal dorsal horn neurons and increased PKCγ protein level in the cytosol. Following the treatment with the opioid receptor antagonist naloxone methiodide (5mg/kg, s.c.), the administration of ketanserin failed to inhibit the repeated inflammation-induced increase in NADPH-d reactivity and c-Fos expression in the spinal dorsal horn. These results suggest that 5-HT2A receptor bioactivity in the inflammatory site plays an important role in repeated inflammation-induced central sensitization. The present study supports the notion that targeting 5-HT2A receptors in the periphery can be a promising therapy for relieving chronic inflammatory pain.
[Mh] Termos MeSH primário: Inflamação/metabolismo
Células do Corno Posterior/efeitos dos fármacos
Receptor 5-HT2A de Serotonina/metabolismo
Antagonistas do Receptor 5-HT2 de Serotonina/farmacologia
Medula Espinal/citologia
[Mh] Termos MeSH secundário: Animais
Carragenina/toxicidade
Regulação da Expressão Gênica/efeitos dos fármacos
Inflamação/induzido quimicamente
Ketanserina/toxicidade
Masculino
NADH Desidrogenase/metabolismo
Óxido Nítrico Sintase/metabolismo
Proteína Quinase C/metabolismo
Ratos
Ratos Sprague-Dawley
Antagonistas do Receptor 5-HT2 de Serotonina/uso terapêutico
Medula Espinal/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, Serotonin, 5-HT2A); 0 (Serotonin 5-HT2 Receptor Antagonists); 9000-07-1 (Carrageenan); 97F9DE4CT4 (Ketanserin); EC 1.14.13.39 (Nitric Oxide Synthase); EC 1.6.99.3 (NADH Dehydrogenase); EC 2.7.1.- (protein kinase C gamma); EC 2.7.11.13 (Protein Kinase C)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160405
[St] Status:MEDLINE


  10 / 2896 MEDLINE  
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[PMID]:26944908
[Au] Autor:Selli C; Tosun M
[Ad] Endereço:Department of Pharmacology, Faculty of Pharmacy, Ege University, 35040, Izmir, Turkey. cigdemselli@gmail.com.
[Ti] Título:Effects of cyclopiazonic acid and dexamethasone on serotonin-induced calcium responses in vascular smooth muscle cells.
[So] Source:J Physiol Biochem;72(2):245-53, 2016 Jun.
[Is] ISSN:1877-8755
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:We previously observed that sarcoendoplasmic reticulum Ca(2+) ATPase (SERCA) blockade by cyclopiazonic acid (CPA) significantly potentiates serotonin (5-hydroxytryptamine (5-HT))-induced vascular contractions. Furthermore, 5-HT receptor antagonist methysergide partially inhibited CPA-potentiated 5-HT contractions. In the present study, we further investigated whether SERCA inhibition potentiates 5-HT-induced Ca(2+) responses along with attenuating the receptor antagonism by store-operated Ca(2+) (SOC) entry and protein kinase C (PKC)-mediated mechanisms. The effects of dexamethasone that was previously shown to induce SOC entry and enhance 5-HT responses were also tested. For this purpose, intracellular Ca(2+) levels were monitored in A7r5 embryonic rat vascular smooth muscle cells by spectrofluorometry using the fluorescent indicator fura-2. The results showed that CPA, although not dexamethasone, significantly potentiated 5-HT-induced Ca(2+) elevations. Ketanserin partially decreased 5-HT-induced and CPA-potentiated Ca(2+) elevations whereas both PKC inhibitor D-sphingosine and SOC entry blocker 2-aminoethoxydiphenyl borate (2-APB) abolished the remaining responses. The data suggests that diminished antagonistic effect on 5-HT-induced Ca(2+) elevations in the presence of SERCA inhibition is induced by SOC entry and PKC activation.
[Mh] Termos MeSH primário: Sinalização do Cálcio/efeitos dos fármacos
Inibidores Enzimáticos/farmacologia
Indóis/farmacologia
Músculo Liso Vascular/efeitos dos fármacos
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/antagonistas & inibidores
Agonistas de Receptores de Serotonina/farmacologia
Serotonina/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/química
Anti-Inflamatórios/farmacologia
Bloqueadores dos Canais de Cálcio/farmacologia
Linhagem Celular
Dexametasona/antagonistas & inibidores
Dexametasona/farmacologia
Inibidores Enzimáticos/química
Indóis/antagonistas & inibidores
Ketanserina/farmacologia
Metisergida/farmacologia
Músculo Liso Vascular/metabolismo
Proteína Quinase C/antagonistas & inibidores
Proteína Quinase C/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Ratos
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo
Serotonina/química
Antagonistas da Serotonina/farmacologia
Agonistas de Receptores de Serotonina/química
Vasoconstritores/antagonistas & inibidores
Vasoconstritores/farmacologia
Vasodilatadores/antagonistas & inibidores
Vasodilatadores/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Calcium Channel Blockers); 0 (Enzyme Inhibitors); 0 (Indoles); 0 (Protein Kinase Inhibitors); 0 (Serotonin Antagonists); 0 (Serotonin Receptor Agonists); 0 (Vasoconstrictor Agents); 0 (Vasodilator Agents); 333DO1RDJY (Serotonin); 7S5I7G3JQL (Dexamethasone); 97F9DE4CT4 (Ketanserin); EC 2.7.11.13 (Protein Kinase C); EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases); X9TLY4580Z (cyclopiazonic acid); XZA9HY6Z98 (Methysergide)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170306
[Lr] Data última revisão:
170306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160306
[St] Status:MEDLINE
[do] DOI:10.1007/s13105-016-0474-8



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