Literatura académica sobre el tema "P2X3"
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Artículos de revistas sobre el tema "P2X3"
Ruan, Huai-Zhen, Lori A. Birder, William C. de Groat, Changfeng Tai, James Roppolo, Charles A. Buffington y Geoffrey Burnstock. "Localization of P2X and P2Y Receptors in Dorsal Root Ganglia of the Cat". Journal of Histochemistry & Cytochemistry 53, n.º 10 (27 de junio de 2005): 1273–82. http://dx.doi.org/10.1369/jhc.4a6556.2005.
Texto completoCoutinho-Silva, Robson, Lynn Stahl, Kwok-Kuen Cheung, Nathalia Enes de Campos, Carolina de Oliveira Souza, David M. Ojcius y Geoffrey Burnstock. "P2X and P2Y purinergic receptors on human intestinal epithelial carcinoma cells: effects of extracellular nucleotides on apoptosis and cell proliferation". American Journal of Physiology-Gastrointestinal and Liver Physiology 288, n.º 5 (mayo de 2005): G1024—G1035. http://dx.doi.org/10.1152/ajpgi.00211.2004.
Texto completoRuan, Huai Zhen, Lori A. Birder, Zhenghua Xiang, Bikramjit Chopra, Tony Buffington, Changfeng Tai, James R. Roppolo, William C. de Groat y Geoffrey Burnstock. "Expression of P2X and P2Y receptors in the intramural parasympathetic ganglia of the cat urinary bladder". American Journal of Physiology-Renal Physiology 290, n.º 5 (mayo de 2006): F1143—F1152. http://dx.doi.org/10.1152/ajprenal.00333.2005.
Texto completoChen, Lin, Changlong Leng, Qin Ru, Qi Xiong, Mei Zhou y Yuxiang Wu. "Retrograde Labeling of Different Distribution Features of DRG P2X2 and P2X3 Receptors in a Neuropathic Pain Rat Model". BioMed Research International 2020 (23 de julio de 2020): 1–15. http://dx.doi.org/10.1155/2020/9861459.
Texto completoBirder, L. A., H. Z. Ruan, B. Chopra, Z. Xiang, S. Barrick, C. A. Buffington, J. R. Roppolo, A. P. D. W. Ford, W. C. de Groat y G. Burnstock. "Alterations in P2X and P2Y purinergic receptor expression in urinary bladder from normal cats and cats with interstitial cystitis". American Journal of Physiology-Renal Physiology 287, n.º 5 (noviembre de 2004): F1084—F1091. http://dx.doi.org/10.1152/ajprenal.00118.2004.
Texto completoBaines, Abigail, Katie Parkinson, Joan A. Sim, Laricia Bragg, Christopher R. L. Thompson y R. Alan North. "Functional Properties of Five Dictyostelium discoideum P2X Receptors". Journal of Biological Chemistry 288, n.º 29 (5 de junio de 2013): 20992–1000. http://dx.doi.org/10.1074/jbc.m112.445346.
Texto completoStoop, Ron, Annmarie Surprenant y R. Alan North. "Different Sensitivities to pH of ATP-Induced Currents at Four Cloned P2X Receptors". Journal of Neurophysiology 78, n.º 4 (1 de octubre de 1997): 1837–40. http://dx.doi.org/10.1152/jn.1997.78.4.1837.
Texto completoLee, B. M., H. Jo, G. Park, Y. H. Kim, C. K. Park, S. J. Jung, G. Chung y S. B. Oh. "Extracellular ATP Induces Calcium Signaling in Odontoblasts". Journal of Dental Research 96, n.º 2 (2 de octubre de 2016): 200–207. http://dx.doi.org/10.1177/0022034516671308.
Texto completoNakamura, Ei'Ichiro, Yasuhito Uezono, Ken'Ichiro Narusawa, Izumi Shibuya, Yosuke Oishi, Masahiro Tanaka, Nobuyuki Yanagihara, Toshitaka Nakamura y Futoshi Izumi. "ATP activates DNA synthesis by acting on P2X receptors in human osteoblast-like MG-63 cells". American Journal of Physiology-Cell Physiology 279, n.º 2 (1 de agosto de 2000): C510—C519. http://dx.doi.org/10.1152/ajpcell.2000.279.2.c510.
Texto completoSamways, Damien S. K. y Terrance M. Egan. "Acidic Amino Acids Impart Enhanced Ca2+ Permeability and Flux in Two Members of the ATP-gated P2X Receptor Family". Journal of General Physiology 129, n.º 3 (26 de febrero de 2007): 245–56. http://dx.doi.org/10.1085/jgp.200609677.
Texto completoTesis sobre el tema "P2X3"
Schiavuzzo, Jalile Garcia 1980. "Mecanismos envolvidos na ação hiperalgésica induzida pela ativação de receptores P2X3 e P2X2/3 no músculo gastrocnêmio de ratos". [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/244518.
Texto completoDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Aplicadas
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Resumo: Existem evidências do envolvimento do ATP via ativação do receptor P2X3 na dor muscular. Portanto, o objetivo deste estudo foi verificar se a ativação do receptor P2X3 no músculo gastrocnêmio de ratos induz hiperalgesia mecânica, e em caso afirmativo, analisar os mecanismos inflamatórios pelo qual os receptores P2x3 induzem hiperalgesia mecânica. O Antagonista não seletivo para o receptor P2X3 ?,?meATP foi administrado no músculo gastrocnêmio de ratos, induzindo hiperalgesia, a qual foi significativamente reduzida pelo antagonista seletivo do receptor P2X3 e P2X2/3 - A-317491. A hiperalgesia mecânica induzida pelo ?,?meATP foi reduzida pelo inibidor de ciclooxigenase Indometacina, pelo antagonista seletivo do receptor de Bradicinina B1 e B2- Dalbk e Bradyzide, respectivamente, antagonista dos adrenoceptores ?1 e ?2 - Atenolol e ICI 118,551 respectivamente, e inibidor não específico de selectinas Fucoidan. O ?,?meATP também induziu o aumento da concentração local de citocinas pro inflamatórias TNF-?, IL-1?, IL-6 e CIN e migração de neutrófilos. Juntos estes achados sugerem que o ?,?meATP induz hiperalgesia mecânica no músculo gastrocnêmio via ativação de receptor periférico P2X3, o qual envolve bradicinina, prostaglandinas e aminas simpatomiméticas e migração de neutrófilos. Portanto, nós sugerimos que os receptores P2X3 sejam um importante alvo no controle da dor muscular
Abstract: There is evidence of the involvement of endogenous ATP via activation of P2X3 in muscle pain. Therefore, the aim of this study was to verify whether the activation of P2X3 receptors in the gastrocnêmio muscle of rats induces mechanical hyperalgesia and, if so, to analyze the inflammatory mechanisms by which P2X3 receptors induce mechanical hyperalgesia. Intramuscular administration of the non-selective P2X3 receptor agonist ?,?-meATP in the gastrocnemius muscle of rats induced mechanical hyperalgesia, which was significantly reduced by the selective P2X3 and P2X2/3 receptors antagonist A-317491. The ?,?-meATP-induced mechanical hyperalgesia was prevented by the indomethacin cyclooxygenase inhibitor, the selective bradykinin B1- or B2- receptor antagonist DALBK and bradyzide, respectively, the ?1- or ?2-adrenoceptor antagonist atenolol and ICI 118,551, respectively, and the nonspecific selectin inhibitor fucoidan. ?,?-meATP also induced increase in the local concentration of the pro-inflammatory cytokines TNF-?, IL-1?, IL-6 and CINC-1 and the neutrophil migration. Together, these findings suggest that ?,?-meATP induced mechanical VIII hyperalgesia in the gastrocnemius muscle of rats via activation of peripheral P2X3 receptors, which involves bradykinin, prostaglandins, sympathetic amines, pro-inflammatory cytokines and neutrophil migration. Therefore, we suggest that P2X3 receptors are important targets to control muscle inflammatory pain
Mestrado
Biodinâmica do Movimento Humano e Esporte
Mestra em Ciências da Nutrição e do Esporte e Metabolismo
Chabot-Doré, Anne-Julie. "Metabotropic regulation of ATP-gated P2X3 receptors". Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101708.
Texto completoWang, Haihong. "Amino acid residues constituting the agonist binding site of the human P2X3 receptor and subunit stoichiometry of heteromeric P2X2/3 and P2X2/6 receptors". Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-112913.
Texto completoMo, Gary. "Molecular physiology of sensory P2X3 ATP receptor channels". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107793.
Texto completoIl a été montré que la transmission purinergique médiée par la libération extracellulaire d'ATP est impliquée dans de nombreux processus physiologiques, allant du fonctionnement de la vessie aux sens du goût et de l'audition. Les rôles variés de la signalisation par l'ATP sont expliqués principalement par la distribution étendue des récepteurs P2 de l'ATP dans l'organisme. Depuis leur clonage initial dans les années '90, une variété de récepteurs P2 régissant divers mécanismes cellulaires a été découverte dans plusieurs tissus. Un récepteur canal P2 en particulier, P2X3, se trouve exprimé quasi-exclusivement dans les neurones nocicepteurs des ganglions spinaux (DRG). De par cette distribution spécifique, le récepteur P2X3 est une cible importante dans la recherche sur la douleur, principalement dans les études sur la douleur chronique. De nombreuses études indiquent le rôle du récepteur P2X3 dans l'augmentation des réponses à la douleur associée à une inflammation chronique ou une lésion neuropathique. Cependant, la contribution exacte de P2X3 dans la douleur chronique reste incertaine, surtout dans les cas de douleur neuropathqiue. Il existe des contradictions dans les articles sur les changements d'expression ou d'activité de P2X3 en conditions de douleur neuropathique. Un élément clé dans l'exacerbation des comportements douloureux après lésion neuropathique est l'augmentation d'excitabilité des neurones sensoriels. La première étude décrite dans cette thèse explore la contribution de P2X3 dans les changements d'excitabilité des neurones de DRG endommagé. Il a été rapporté que l'activation de la protéine kinase C (PKC) facilite les comportements douloureux en modulant l'activité de certains canaux ioniques. Ainsi, la contribution de PKC à l'hyperexcitabilité des neurones de DRG neuropathique a aussi été étudiée dans ce premier chapitre. Une insulte à un nerf périphérique induit des changements très dynamiques dans sa physiologie cellulaire, incluant l'activation de voies de signalisation intracellulaires. La fonction de P2X3 peut se trouver affectée par ces mécanismes neuronaux. Comprendre la physiologie moléculaire du récepteur P2X3 peut nous éclairer sur sa contribution spécifique dans la douleur. Une étape commune à de nombreuses voies de signalisation cellulaire est le clivage du phosphatidylinositol 4,5-bisphosphate (PIP2) par la phospholipase C (PLC). Les variations de niveaux de PIP2 modulent l'activité de plusieurs canaux ioniques, y compris le récepteur P2X2. Le deuxième chapitre dans cette thèse se concentre sur la modulation de P2X3 par les niveaux intracellulaires de PIP2. Des études récentes ont démontré la co-expression potentielle de récepteurs métabotropiques P2Y et ionotropiques P2X3 sur les neurones sensoriels. L'ATP pouvant activer les deux types de récepteurs, le troisième chapitre se penche sur la modulation de la fonction de P2X3 par les récepteurs P2Y couplés à la phospholipase C.Notre compréhension du récepteur P2X3 provient principalement des données obtenues dans des modèles précliniques de rongeurs. Sachant que des différences interspécifiques marquées dans les propriétés fonctionnelles de certains sous-types de récepteurs P2X ont été documentées, il est urgent et important de vérifier que nos connaissances sur le récepteur P2X3 de rongeur sont transférables aux primates ou à l'homme. À cette fin, dans la dernière étude de cette thèse, nous comparons les propriétés pharmacologiques du récepteur P2X3 natif à la surface des neurones sensoriels de rat avec celles du récepteur P2X3 exprimé dans les neurones sensoriels de singe.
Günther, Janka [Verfasser]. "Generierung und Charakterisierung transgener BAC-P2X3-Mäuse / Janka Günther". Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2014. http://d-nb.info/1051414172/34.
Texto completoTeixeira, Juliana Maia 1984. "Involvement of P2X3 and P2X7 purinergic receptors in inflammatory articular hyperalgesia in the knee joint of rats and the study of the peripheral mechanisms involved = Participação dos receptores purinérgicos P2X3 e P2X7 na hiperalgesia inflamatória articular em joelho de ratos e o estudo dos mecanismos periféricos envolvidos". [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314054.
Texto completoTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: A osteoartrite (OA) é uma doença degenerativa e progressiva, caracterizada pela degradação da cartilagem que reveste as extremidades ósseas e inflamação da membrana sinovial, causando incapacidade física, inchaço articular e dor. Embora o alívio da dor severa seja o principal objetivo no tratamento agudo, pouco se sabe sobre os mecanismos envolvidos no desenvolvimento da dor na OA. Estudos demonstram a participação do ATP (adenosina 5¿-trifosfato) em processos de hiperalgesia através da ativação dos receptores purinérgicos P2X3, P2X2/3 e P2X7. Portanto, os objetivos deste estudo foram: (1) investigar a participação dos receptores P2X3, P2X2/3 e P2X7 na hiperalgesia articular em modelo de artrite na articulação do joelho de ratos machos e fêmeas em estro e se há diferenças sexuais no efeito induzido pelos antagonistas de receptores P2X3, P2X2/3 e P2X7. (2) testar a hipótese de que a inflamação articular induzida pela carragenina aumenta a expressão do receptor P2X3 nos condrócitos da cartilagem articular da articulação do joelho de ratos. (3) verificar se o mecanismo pelo qual a ativação dos receptores P2X3, P2X2/3 e P2X7 contribui para a hiperalgesia articular depende da liberação prévia de citocinas pró-inflamatórias e da migração de neutrófilos. (4) investigar se a ativação dos receptores P2X3, P2X2/3 e P2X7 induz hiperalgesia na articulação do joelho de ratos dependente da liberação de mediadores inflamatórios. (5) testar a hipótese de que a ativação dos receptores P2X3, P2X2/3 e P2X7 contribui para a hiperalgesia articular induzida pelos mediadores inflamatórios: bradicinina, citocinas pró-inflamatórias, PGE2 e dopamina. Para os objetivos 1, 4 e 5, a hiperalgesia articular foi quantificada através do teste de Incapacitação Articular. Para o objetivo 2, foi utilizado o ensaio de imunofluorescência. Para os objetivos 3 e 4 foram utilizados os ensaios imuno-enzimáticos ELISA e MPO. Os resultados demonstram que a ativação dos receptores P2X3, P2X2/3 e P2X7 pelo ATP endógeno é essencial para o desenvolvimento da hiperalgesia articular induzida pela carragenina na articulação do joelho de ratos machos e fêmeas em estro, que são mais sensíveis do que os machos aos efeitos anti-hiperalgésicos e anti-inflamatórios induzidos pelo antagonista de receptor P2X7. Durante a inflamação articular induzida pela carragenina ocorre um aumento na expressão dos receptores P2X3 nos condrócitos da cartilagem articular. O papel dos receptores P2X3, P2X2/3 e P2X7 na hiperalgesia articular é mediado pela sensibilização indireta dos nociceptores aferentes primários, dependente da liberação prévia de citocinas pró-inflamatórias e da migração de neutrófilos. Além disso, a ativação dos receptores P2X3, P2X2/3 e P2X7 induz hiperalgesia articular dependente da liberação de bradicinina, aminas simpatomiméticas, prostaglandinas e citocinas pró-inflamatórias. Finalmente, a hiperalgesia articular induzida pelos mediadores inflamatórios bradicinina, PGE2 e dopamina depende da ativação de receptores P2X3 e P2X2/3, enquanto que a ativação de receptor P2X7 contribui para a hiperalgesia articular induzida pela bradicinina e dopamina. Concluindo, os resultados apresentados sugerem que os receptores P2X3, P2X2/3 e P2X7 são alvos farmacológicos interessantes para o tratamento das doenças inflamatórias articulares como a osteoartrite. Particularmente em relação ao receptor P2X7, antagonistas seletivos podem ser usados para reduzir a dor e inflamação no joelho, especialmente em mulheres
Abstract: Osteoarthritis (OA) is a degenerative and progressive disease, characterized by cartilage breakdown which covers the bone ends and by synovial membrane inflammation, causing disability, joint swelling and pain. The relief of severe pain is the main goal of the acute treatment, but little is known about the mechanisms involved in the development of pain in OA. It has been demonstrated the role of ATP (adenosine 5'-triphosphate) in processes of hyperalgesia through activation of purinergic receptors P2X3, P2X2/3 and P2X7. Therefore, the aims of this study were: (1) to investigate the role of P2X3, P2X2/3 and P2X7 receptors in articular hyperalgesia in the knee joint arthritis model in males and estrus females rats and, if so, whether there are sex differences in the effect induced by the selective P2X3, P2X2/3 and P2X7 receptors antagonists. (2) to test the hypothesis that the carrageenan-induced articular inflammation increases the expression of P2X3 receptor in chondrocytes of articular cartilage of the knee joint. (3) to verify whether the mechanism by which the P2X3, P2X2/3 and P2X7 receptors activation contributes to articular hyperalgesia depends on previous pro-inflammatory cytokines release and neutrophil migration. (4) to investigate whether the P2X3, P2X2/3 and P2X7 receptors activation induces articular hyperalgesia in the rat¿s knee joint which depends on release of inflammatory mediators. (5) to verify whether the activation of P2X3, P2X2/3 and P2X7 receptors contributes to the articular hyperalgesia induced by the inflammatory mediators bradykinin, pro-inflammatory cytokines, PGE2 and dopamine. For the aims 1, 4 and 5, the articular hyperalgesia was quantified by the rat knee joint Incapacitation Test. The immuno?uorescence method was used for the aim 2. For aims 3 and 4, the ELISA and MPO immunoenzymatic assays were used. The results demonstrate that P2X3, P2X2/3 and P2X7 receptors activation by endogenous ATP is essential for the development of carrageenan-induced articular hyperalgesia in the knee joint of male and estrus female rats, which are more sensitive than males to anti-hyperalgesic and anti-inflammatory effects induced by the P2X7 receptor antagonist. During carrageenan-induced joint inflammation occurs an increased of P2X3 receptors expression in chondrocytes of the articular cartilage. The essential role played by P2X3, P2X2/3 and P2X7 receptors in the development of articular hyperalgesia is mediated by an indirect sensitization of the primary afferent nociceptors dependent on the previous pro-inflammatory cytokines release and neutrophil migration. Moreover, the P2X3, P2X2/3 and P2X7 receptors activation induces articular hyperalgesia which depends on bradykinin, sympathomimetic amines, prostaglandins and pro-inflammatory cytokines release. Finally, the articular hyperalgesia induced by inflammatory mediators bradykinin, PGE2 and dopamine depends on the P2X3 and P2X2/3 receptors activation, while the P2X7 receptor activation contributes to the bradykinin- and dopamine-induced articular hyperalgesia. In conclusion, our results suggest that P2X3, P2X2/3 and P2X7 receptors are interesting pharmacological targets for the treatment of inflammatory joint diseases such as osteoarthritis. In particular, selective P2X7 receptor antagonists can be used to reduce inflammation and pain in the knee joint, especially in women
Doutorado
Fisiologia
Doutora em Biologia Funcional e Molecular
Rashed, Mahmoud [Verfasser]. "Syntheses and structure-activity relationships of novel P2X3 receptor antagonists / Mahmoud Rashed". Bonn : Universitäts- und Landesbibliothek Bonn, 2018. http://d-nb.info/1160594392/34.
Texto completoPrado, Filipe César do. "Papel do receptor P2X3 e da ativação da proteína kinase C épsilon dos neurônios nociceptivos periféricos na dor inflamatória". [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314727.
Texto completoDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Enquanto a hiperalgesia inflamatória depende da liberação de prostaglandinas e/ou de aminas simpatomiméticas que sensibilizam os neurônios aferentes primários, nosso grupo demonstrou recentemente que o bloqueio do receptor P2X3 no tecido periférico previne a hiperalgesia induzida pela carragenina.. No entanto, o mecanismo pelo qual a ativação dos receptores P2X3 neuronais contribui para a hiperalgesia inflamatória não está completamente estabelecido. O presente estudo verifica se a ativação do receptor P2X3 dos neurônios aferentes primários contribui para a hiperalgesia mecânica induzida pela prostaglandina E2 ou pela dopamine no tecido periférico. A co-administração de A317491 (60 µg / paw), um antagonista seletivo do receptor P2X3, ou o prétratamento com dexametasona (1 mg / mL / kg), preveniu a hiperalgesia mecânica medida 3 horas depois da administraçao de carragenina (300 µg / paw) na pata posterior de ratos. A administração de ??meATP (50 µg /paw) induziu hiperalgesia mecânica 1 hora, mas não 3 horas, depois da sua administração, que foi prevenida pela dexametasona ou pelo A317491. Doses sublimiares de PGE2 (4 ng / paw) ou dopamina (0.4 µg / paw) que não induzem hiperalgesia por si só, induziram hiperalgesia, 3 horas depois, quando administradas logo depois de ??meATP ou carragenina em ratos tratados com dexametasona. Esses estados de hiperalgesia ("priming") revelados pelas doses sublimiares de PGE2 ou dopamine foram prevenidos pelo A317491 ou pelo tratamento com administração intraganglionar (DRG-L5) de ODN antisense, mas não pelo ODN mismatch, contra o receptor P2X3 (40 µg /5µL once a day for 4 days). ODN antisense, mas não o ODN mismatch, reduziu a expressão dos receptores P2X3 no nervo safeno e no DRG-L5. Para verificar se a PKC? media esse estado de hiperalgesia, inibidor de translocação de PKC? (1 µg/paw) foi administrado no tecido periférico 45 minutos antes do ??meATP ou PGE2 (100 ng/paw). O inibidor de PKC? preveniu o estado de hiperalgesia induzido pelo ??meATP ("priming"), mas não a hiperalgesia mecânica induzida pela PGE2 (100 ng/paw). Dessa maneira, os resultados desse estudo sugerem que a hiperalgesia inflamatória depended a ativação dos receptores P2X3 neuronais e da subsequente translocação da PKC? , que aumenta a susceptibilidade dos neurônios aferentes primários (priming) à ação de outros mediadores inflamatórios como a PGE2 e as aminas simpatomiméticas
Abstract: While inflammatory hyperalgesia depends on the release of prostaglandins and/or sympathetic amines that ultimately sensitize the primary afferent neurons, we have recently demonstrated that blockade of P2X3 receptor in the peripheral tissue completely prevents carrageenan-induced hyperalgesia. However, the mechanism by which the activation of neuronal P2X3 receptor contributes to the inflammatory hyperalgesia is not completely clear. The present study verifies whether the activation of P2X3 receptor on primary afferent neurons contributes to the mechanical hiperalgesia induced by prostaglandin E2 or dopamine in the peripheral tissue. Co-administration of A317491(60 µg / paw), a selective P2X3,2/3 receptor antagonist, or pre-treatment with dexamethasone (1 mg / mL / Kg), prevented the mechanical hyperalgesia measured 3 hours after the administration of carrageenan (300 µg / paw) in the rat's hind paw. The administration of ??meATP (50 µg /paw) induced mechanical hiperalgesia 1 hour, but not 3 hours, after its administration, which also was prevented by dexamethasone or A317491. Sub-threshold doses of PGE2 (4 ng / paw) or dopamine (0.4 µg / paw) that do not induce hyperalgesia by themselves, induced maximal hyperalgesia, 3 hours after, when administrated Just following ??meATP or carrageenan in rats treated with dexamethasone. These hyperalgesic states ("priming") revealed by sub-threshold doses of PGE2 or dopamine were prevented by A317491 or treatment with ganglionar administrations (DRG-L5) of ODN antisense, but not ODN mismatch, against P2X3 receptor (40 µg /5µL once a day for 4 days). ODN antisense, but not ODN mismatch reduced the expression of P2X3 receptors in the saphenous nerve and in DRG-L5. To verify whether PKC? mediates this hyperalgesic state, PKC? translocation inhibitor (1 µg/paw) was administrated in peripheral tissue 45 min. before ??meATP or PGE2 (100 ng/paw). PKC? inhibitor inhibited the hyperalgesic state induced by ??meATP ("priming"), but not the mechanical hyperalgesia induced by PGE2 (100 ng/paw). Briefly, the findings of this study suggest that the inflammatory hyperalgesia depends on neuronal activation of P2X3 receptor and the subsequent PKC? translocation, which increases the susceptibility of primary afferent neurons (priming) to others inflammatory mediators such as PGE2 and symphatetic amines
Mestrado
Fisiologia
Mestre em Biologia Funcional e Molecular
Chen, Zhicheng. "Molecular cloning and characterisation of a sensory neuron-specific ATP-gated channel (P2X3)". Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285158.
Texto completoHelms, Nick. "Wechselwirkungen von Agonisten und kompetitiven Antagonisten mit der Ligandenbindungsstelle des schnell desensitisierenden P2X3-Rezeptors". Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-197364.
Texto completoLibros sobre el tema "P2X3"
Nicke, Annette, ed. The P2X7 Receptor. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2384-8.
Texto completoVillars, P. y K. Cenzual, eds. Structure Types. Part 2: Space Groups (218) P-43n - (195) P23. Berlin/Heidelberg: Springer-Verlag, 2005. http://dx.doi.org/10.1007/b11233.
Texto completoUnited States. Bureau of the Census, ed. Current Population Reports, Poverty Among Families: etc., Special Studies, 1998, P23-203, Issued September 2000. [S.l: s.n., 2000.
Buscar texto completoCV, Panca Bhakti, ed. Himpunan peraturan perundang-undangan keselamatan dan kesehatan kerja: Dilengkapi dengan Pedoman Operasional Panitia Pembina Keselamatan dan Kesehatan Kerja (P2K3). Jakarta: Panca Bhakti, 2008.
Buscar texto completoFairbairn, Ian Paul. Investigations of a novel mechanism of anti-tuberculous immunity mediated by purinergic (P2X[inferior seven]) receptors. Birmingham: University of Birmingham, 2001.
Buscar texto completoYeung, Davy. Molecular and functional analysis of the purinergic P2X receptors in normal and dystrophic skeletal muscle: A thesis. Portsmouth: University of Portsmouth, School of Pharmacy and Biomedical Sciences, 2004.
Buscar texto completoNicke, Annette. P2X7 Receptor: Methods and Protocols. Springer, 2022.
Buscar texto completoKopanski, Tomasz J. PZL P23 Karas. Mushroom Model Publications,Poland, 2004.
Buscar texto completoZalewski, Sharon. How Should Drugs Be Legally Prescribed (P213). Greenhaven Press, 1988.
Buscar texto completoLau, Chung-Ming, Chi-Sum Wong, Kenneth K. S. Law y David K. Tse. Asian Management Matters. PUBLISHED BY IMPERIAL COLLEGE PRESS AND DISTRIBUTED BY WORLD SCIENTIFIC PUBLISHING CO., 2000. http://dx.doi.org/10.1142/p203.
Texto completoCapítulos de libros sobre el tema "P2X3"
Kennedy, Charles. "P2X3 Receptors and Sensory Transduction". En Sensing with Ion Channels, 247–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-72739-2_12.
Texto completoFabbretti, Elsa. "ATP-Gated P2X3 Receptors Are Specialised Sensors of the Extracellular Environment". En Advances in Experimental Medicine and Biology, 7–16. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/5584_2017_56.
Texto completoSluyter, Ronald. "The P2X7 Receptor". En Advances in Experimental Medicine and Biology, 17–53. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/5584_2017_59.
Texto completoEvans, Richard J., Annmarie Surprenant y R. Alan North. "P2X Receptors". En The P2 Nucleotide Receptors, 43–61. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4612-1800-5_2.
Texto completoChessell, I. P., A. D. Michel y P. P. A. Humphrey. "P2X Receptors". En Purinergic and Pyrimidinergic Signalling I, 47–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-662-09604-8_3.
Texto completoKawate, Toshimitsu. "P2X Receptor Activation". En Advances in Experimental Medicine and Biology, 55–69. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/5584_2017_55.
Texto completoShen, Jian-Bing, Bruce T. Liang y Florentina Soto. "Nucleotide Receptor P2x". En Encyclopedia of Signaling Molecules, 3616–29. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_50.
Texto completoRehn, Alexandra Beatrice y Johannes Buchner. "p23 and Aha1". En Subcellular Biochemistry, 113–31. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-11731-7_6.
Texto completoHorstkorte, Rüdiger, Bettina Büttner, Kaya Bork, Navdeep Sahota, Sarah Sabir, Laura O’Regan, Joelle Blot et al. "Nucleotide Receptor P2x". En Encyclopedia of Signaling Molecules, 1275–87. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_50.
Texto completoRassendren, François y Lauriane Ulmann. "P2X Receptors and Pain". En Pathologies of Calcium Channels, 615–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40282-1_30.
Texto completoActas de conferencias sobre el tema "P2X3"
Wortley, Michael, Eric Dubuis, Sarah Maher, Sara Bonvini, Mark Birrell y Maria Belvisi. "TRPM3, P2X2 and P2X3 expression patterns in single airway sensory nerves". En ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa4411.
Texto completoSmith, Jaclyn y Rachel Giles. "Novel P2X3 antagonist can SOOTHE chronic cough". En ATS 2022 International Conference, editado por Richard Dekhuijzen. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/7e412546.
Texto completoFriedrich, Christian, Klaus Francke, Surinder S. Birring, J. W. K. Van Den Berg, Paul Marsden, Lorcan Mcgarvey, Alice Turner et al. "Safety and efficacy of P2X3 antagonist BAY 1902607 in refractory chronic cough". En ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.4566.
Texto completoMartinez, F. J., A. Afzal, M. M. Kitt, A. Ford, J. J. Li, Y. P. Li y J. Smith. "The Treatment of Chronic Cough in Idiopathic Pulmonary Fibrosis Patients with Gefapixant, a P2x3 Receptor Antagonist". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2638.
Texto completoBirrell, Mark, Sara J. Bonvini, Katie E. Baker, Bilel Dekkak, Anthony Ford, Montse Miralpeix, Gema Tarrason, Jaclyn A. Smith y Maria G. Belvisi. "Central role for the TRPV4-ATP-P2X3 axis in sensory nerve activation and the late asthmatic response". En ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa5069.
Texto completoGarceau, D., N. Chauret y L. Harvey. "BLU-5937 a Highly Selective P2X3 Homotrimeric Receptor Antagonist with Improved Taste Safety Profile in Healthy Subjects". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7396.
Texto completoMorice, A. H., J. Smith, L. McGarvey, S. Birring, S. M. Parker, A. Turner, I. Gashaw et al. "Safety and Efficacy of BAY 1817080, a P2X3 Receptor Antagonist, in Patients with Refractory Chronic Cough (RCC)". En American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7648.
Texto completoIshihara, Hiroyuki, Hideaki Hida, Mitsuaki Machida, Yoshiyuki Tsuda y Sayaka Miyazaki. "Design of phase 2b randomised controlled trial of S-600918, P2X3 receptor antagonist for refractory chronic cough". En ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2271.
Texto completoSmith, Jaclyn, Lorcan P. Mcgarvey, Alyn H. Morice, Surinder S. Birring, Michael M. Kitt, Mandel R. Sher, Andrew M. Tershakovec, Wen-Chi Wu, Zhi Jin Xu y David R. Muccino. "The effect of baseline factors on treatment response with MK-7264, a P2X3 antagonist, in refractory chronic cough." En ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa811.
Texto completoMcGarvey, Lorcan, Jaclyn Smith, Surinder Birring, Alyn Morice, Mandel Sher, Wen-Chi Wu y David Muccino. "Characterization of chronic cough patients participating in a phase 2b clinical trial of gefapixant, a P2X3 receptor antagonist". En ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa612.
Texto completoInformes sobre el tema "P2X3"
Kimbler, Donald. Therapeutic Targeting of P2X7 after TBI. Fort Belvoir, VA: Defense Technical Information Center, noviembre de 2012. http://dx.doi.org/10.21236/ada616284.
Texto completoDawson, William O. y Moshe Bar-Joseph. Creating an Ally from an Adversary: Genetic Manipulation of Citrus Tristeza. United States Department of Agriculture, enero de 2004. http://dx.doi.org/10.32747/2004.7586540.bard.
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