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dc.contributor.authorPhelan, Kevin D.es
dc.contributor.authorShwe, U Thaunges
dc.contributor.authorCozart, Michael A.es
dc.contributor.authorWu, Honges
dc.contributor.authorMock, Matthew M.es
dc.contributor.authorAbramowitz, Joeles
dc.contributor.authorBirnbaumer, Lutzes
dc.contributor.authorZheng, Fanges
dc.date.accessioned2019-09-13T18:47:43Z-
dc.date.available2019-09-13T18:47:43Z-
dc.date.issued2017-
dc.identifier.citationPhelan KD, Shwe UT, Cozart MA, et al. TRPC3 channels play a critical role in the theta component of pilocarpine-induced status epilepticus in mice [en línea]. Epilepsia. 2017;58(2):247-254. doi:10.1111/epi.13648 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8738es
dc.identifier.issn0013-9580-
dc.identifier.issn1528-1167 (online)-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/8738-
dc.description.abstractAbstract: Canonical transient receptor potential (TRPC) channels constitute a family of cation channels that exhibit a regional and cell-specific expression pattern throughout the brain. It has been reported previously that TRPC3 channels are effectors of the brain-derived neurotrophic factor (BDNF)/trkB signaling pathway. Given the long postulated role of BDNF in epileptogenesis, TRPC3 channels may be a critical component in the underlying pathophysiology of seizure and epilepsy. In this study, we investigated the precise role of TRPC3 channels in pilocarpine-induced status epilepticus (SE).es
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherWileyes
dc.rightsAcceso Abierto*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.sourceEpilepsia. 2017;58(2):247-254es
dc.subjectELECTROENCEFALOGRAFIAes
dc.subjectNEURONASes
dc.subjectANALISIS ESPECTRALes
dc.subjectSISTEMA NERVIOSOes
dc.subjectMEDICAMENTOSes
dc.subjectEPILEPSIAes
dc.titleTRPC3 channels play a critical role in the theta component of pilocarpine-induced status epilepticus in micees
dc.typeArtículoes
dc.identifier.doi10.1111/epi.13648-
dc.identifier.pmid28012173-
uca.disciplinaMEDICINAes
uca.issnrd1es
uca.affiliationFil: Phelan, Kevin D. University of Arkansas for Medical Sciences. Department of Neurobiology and Developmental Sciences; Estados Unidoses
uca.affiliationFil: Shwe, U Thaung. Universityof Arkansas for Medical Sciences. Department of Pharmacology and Toxicology; Estados Unidoses
uca.affiliationFil: Cozart, Michael A. Universityof Arkansas for Medical Sciences. Department of Pharmacology and Toxicology; Estados Unidoses
uca.affiliationFil: Wu, Hong. Universityof Arkansas for Medical Sciences. Department of Pharmacology and Toxicology; Estados Unidoses
uca.affiliationFil: Mock, Matthew M. Universityof Arkansas for Medical Sciences. Department of Pharmacology and Toxicology; Estados Unidoses
uca.affiliationFil: Abramowitz, Joel. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidoses
uca.affiliationFil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidoses
uca.affiliationFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentinaes
uca.affiliationFil: Zheng, Fang. Universityof Arkansas for Medical Sciences. Department of Pharmacology and Toxicology; Estados Unidoses
uca.versionpublishedVersiones
item.grantfulltextopen-
item.fulltextWith Fulltext-
item.languageiso639-1en-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Función y Farmacología de Canales Iónicos-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.deptFacultad de Ciencias Médicas-
crisitem.author.orcid0000-0002-0775-8661-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgPontificia Universidad Católica Argentina-
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