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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

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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

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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

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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

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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

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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

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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

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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

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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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