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Articles de revues sur le sujet "P2X3"
Ruan, Huai-Zhen, Lori A. Birder, William C. de Groat, Changfeng Tai, James Roppolo, Charles A. Buffington et Geoffrey Burnstock. « Localization of P2X and P2Y Receptors in Dorsal Root Ganglia of the Cat ». Journal of Histochemistry & ; Cytochemistry 53, no 10 (27 juin 2005) : 1273–82. http://dx.doi.org/10.1369/jhc.4a6556.2005.
Texte intégralCoutinho-Silva, Robson, Lynn Stahl, Kwok-Kuen Cheung, Nathalia Enes de Campos, Carolina de Oliveira Souza, David M. Ojcius et 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, no 5 (mai 2005) : G1024—G1035. http://dx.doi.org/10.1152/ajpgi.00211.2004.
Texte intégralRuan, Huai Zhen, Lori A. Birder, Zhenghua Xiang, Bikramjit Chopra, Tony Buffington, Changfeng Tai, James R. Roppolo, William C. de Groat et 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, no 5 (mai 2006) : F1143—F1152. http://dx.doi.org/10.1152/ajprenal.00333.2005.
Texte intégralChen, Lin, Changlong Leng, Qin Ru, Qi Xiong, Mei Zhou et 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 juillet 2020) : 1–15. http://dx.doi.org/10.1155/2020/9861459.
Texte intégralBirder, 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 et 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, no 5 (novembre 2004) : F1084—F1091. http://dx.doi.org/10.1152/ajprenal.00118.2004.
Texte intégralBaines, Abigail, Katie Parkinson, Joan A. Sim, Laricia Bragg, Christopher R. L. Thompson et R. Alan North. « Functional Properties of Five Dictyostelium discoideum P2X Receptors ». Journal of Biological Chemistry 288, no 29 (5 juin 2013) : 20992–1000. http://dx.doi.org/10.1074/jbc.m112.445346.
Texte intégralStoop, Ron, Annmarie Surprenant et R. Alan North. « Different Sensitivities to pH of ATP-Induced Currents at Four Cloned P2X Receptors ». Journal of Neurophysiology 78, no 4 (1 octobre 1997) : 1837–40. http://dx.doi.org/10.1152/jn.1997.78.4.1837.
Texte intégralLee, B. M., H. Jo, G. Park, Y. H. Kim, C. K. Park, S. J. Jung, G. Chung et S. B. Oh. « Extracellular ATP Induces Calcium Signaling in Odontoblasts ». Journal of Dental Research 96, no 2 (2 octobre 2016) : 200–207. http://dx.doi.org/10.1177/0022034516671308.
Texte intégralNakamura, Ei'Ichiro, Yasuhito Uezono, Ken'Ichiro Narusawa, Izumi Shibuya, Yosuke Oishi, Masahiro Tanaka, Nobuyuki Yanagihara, Toshitaka Nakamura et 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, no 2 (1 août 2000) : C510—C519. http://dx.doi.org/10.1152/ajpcell.2000.279.2.c510.
Texte intégralSamways, Damien S. K., et 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, no 3 (26 février 2007) : 245–56. http://dx.doi.org/10.1085/jgp.200609677.
Texte intégralThèses sur le sujet "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.
Texte intégralDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Aplicadas
Made available in DSpace on 2018-08-24T04:40:35Z (GMT). No. of bitstreams: 1 Schiavuzzo_JalileGarcia_M.pdf: 1205741 bytes, checksum: b599c1bee7cda79ed3554fcb789eea9d (MD5) Previous issue date: 2013
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.
Texte intégralWang, 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.
Texte intégralMo, 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.
Texte intégralIl 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.
Texte intégralTeixeira, 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.
Texte intégralTese (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.
Texte intégralPrado, 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.
Texte intégralDissertação (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.
Texte intégralHelms, 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.
Texte intégralLivres sur le sujet "P2X3"
Nicke, Annette, dir. The P2X7 Receptor. New York, NY : Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2384-8.
Texte intégralVillars, P., et K. Cenzual, dir. Structure Types. Part 2 : Space Groups (218) P-43n - (195) P23. Berlin/Heidelberg : Springer-Verlag, 2005. http://dx.doi.org/10.1007/b11233.
Texte intégralUnited States. Bureau of the Census, dir. Current Population Reports, Poverty Among Families : etc., Special Studies, 1998, P23-203, Issued September 2000. [S.l : s.n., 2000.
Trouver le texte intégralCV, Panca Bhakti, dir. Himpunan peraturan perundang-undangan keselamatan dan kesehatan kerja : Dilengkapi dengan Pedoman Operasional Panitia Pembina Keselamatan dan Kesehatan Kerja (P2K3). Jakarta : Panca Bhakti, 2008.
Trouver le texte intégralFairbairn, Ian Paul. Investigations of a novel mechanism of anti-tuberculous immunity mediated by purinergic (P2X[inferior seven]) receptors. Birmingham : University of Birmingham, 2001.
Trouver le texte intégralYeung, 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.
Trouver le texte intégralNicke, Annette. P2X7 Receptor : Methods and Protocols. Springer, 2022.
Trouver le texte intégralKopanski, Tomasz J. PZL P23 Karas. Mushroom Model Publications,Poland, 2004.
Trouver le texte intégralZalewski, Sharon. How Should Drugs Be Legally Prescribed (P213). Greenhaven Press, 1988.
Trouver le texte intégralLau, Chung-Ming, Chi-Sum Wong, Kenneth K. S. Law et 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.
Texte intégralChapitres de livres sur le sujet "P2X3"
Kennedy, Charles. « P2X3 Receptors and Sensory Transduction ». Dans Sensing with Ion Channels, 247–66. Berlin, Heidelberg : Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-72739-2_12.
Texte intégralFabbretti, Elsa. « ATP-Gated P2X3 Receptors Are Specialised Sensors of the Extracellular Environment ». Dans Advances in Experimental Medicine and Biology, 7–16. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/5584_2017_56.
Texte intégralSluyter, Ronald. « The P2X7 Receptor ». Dans Advances in Experimental Medicine and Biology, 17–53. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/5584_2017_59.
Texte intégralEvans, Richard J., Annmarie Surprenant et R. Alan North. « P2X Receptors ». Dans The P2 Nucleotide Receptors, 43–61. Totowa, NJ : Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4612-1800-5_2.
Texte intégralChessell, I. P., A. D. Michel et P. P. A. Humphrey. « P2X Receptors ». Dans 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.
Texte intégralKawate, Toshimitsu. « P2X Receptor Activation ». Dans Advances in Experimental Medicine and Biology, 55–69. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/5584_2017_55.
Texte intégralShen, Jian-Bing, Bruce T. Liang et Florentina Soto. « Nucleotide Receptor P2x ». Dans Encyclopedia of Signaling Molecules, 3616–29. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_50.
Texte intégralRehn, Alexandra Beatrice, et Johannes Buchner. « p23 and Aha1 ». Dans Subcellular Biochemistry, 113–31. Cham : Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-11731-7_6.
Texte intégralHorstkorte, Rüdiger, Bettina Büttner, Kaya Bork, Navdeep Sahota, Sarah Sabir, Laura O’Regan, Joelle Blot et al. « Nucleotide Receptor P2x ». Dans 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.
Texte intégralRassendren, François, et Lauriane Ulmann. « P2X Receptors and Pain ». Dans Pathologies of Calcium Channels, 615–33. Berlin, Heidelberg : Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40282-1_30.
Texte intégralActes de conférences sur le sujet "P2X3"
Wortley, Michael, Eric Dubuis, Sarah Maher, Sara Bonvini, Mark Birrell et Maria Belvisi. « TRPM3, P2X2 and P2X3 expression patterns in single airway sensory nerves ». Dans ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa4411.
Texte intégralSmith, Jaclyn, et Rachel Giles. « Novel P2X3 antagonist can SOOTHE chronic cough ». Dans ATS 2022 International Conference, sous la direction de Richard Dekhuijzen. Baarn, the Netherlands : Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/7e412546.
Texte intégralFriedrich, 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 ». Dans ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.4566.
Texte intégralMartinez, F. J., A. Afzal, M. M. Kitt, A. Ford, J. J. Li, Y. P. Li et J. Smith. « The Treatment of Chronic Cough in Idiopathic Pulmonary Fibrosis Patients with Gefapixant, a P2x3 Receptor Antagonist ». Dans 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.
Texte intégralBirrell, Mark, Sara J. Bonvini, Katie E. Baker, Bilel Dekkak, Anthony Ford, Montse Miralpeix, Gema Tarrason, Jaclyn A. Smith et Maria G. Belvisi. « Central role for the TRPV4-ATP-P2X3 axis in sensory nerve activation and the late asthmatic response ». Dans ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa5069.
Texte intégralGarceau, D., N. Chauret et L. Harvey. « BLU-5937 a Highly Selective P2X3 Homotrimeric Receptor Antagonist with Improved Taste Safety Profile in Healthy Subjects ». Dans 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.
Texte intégralMorice, 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) ». Dans 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.
Texte intégralIshihara, Hiroyuki, Hideaki Hida, Mitsuaki Machida, Yoshiyuki Tsuda et Sayaka Miyazaki. « Design of phase 2b randomised controlled trial of S-600918, P2X3 receptor antagonist for refractory chronic cough ». Dans ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2271.
Texte intégralSmith, 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 et David R. Muccino. « The effect of baseline factors on treatment response with MK-7264, a P2X3 antagonist, in refractory chronic cough. » Dans ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa811.
Texte intégralMcGarvey, Lorcan, Jaclyn Smith, Surinder Birring, Alyn Morice, Mandel Sher, Wen-Chi Wu et David Muccino. « Characterization of chronic cough patients participating in a phase 2b clinical trial of gefapixant, a P2X3 receptor antagonist ». Dans ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa612.
Texte intégralRapports d'organisations sur le sujet "P2X3"
Kimbler, Donald. Therapeutic Targeting of P2X7 after TBI. Fort Belvoir, VA : Defense Technical Information Center, novembre 2012. http://dx.doi.org/10.21236/ada616284.
Texte intégralDawson, William O., et Moshe Bar-Joseph. Creating an Ally from an Adversary : Genetic Manipulation of Citrus Tristeza. United States Department of Agriculture, janvier 2004. http://dx.doi.org/10.32747/2004.7586540.bard.
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