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dc.contributor.author
Cozart, Michael A.
dc.contributor.author
Phelan, Kevin D.
dc.contributor.author
Wu, Hong
dc.contributor.author
Mu, Shengyu
dc.contributor.author
Birnbaumer, Lutz
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dc.contributor.author
Rusch, Nancy J.
dc.contributor.author
Zheng, Fang
dc.date.available
2021-09-28T13:04:06Z
dc.date.issued
2020-12
dc.identifier.citation
Cozart, Michael A.; Phelan, Kevin D.; Wu, Hong; Mu, Shengyu; Birnbaumer, Lutz; et al.; Vascular smooth muscle TRPC3 channels facilitate the inverse hemodynamic response during status epilepticus; Nature; Scientific Reports; 10; 1; 12-2020; 1-10
dc.identifier.issn
1476-4687
dc.identifier.uri
http://hdl.handle.net/11336/141701
dc.description.abstract
Human status epilepticus (SE) is associated with a pathological reduction in cerebral blood flow termed the inverse hemodynamic response (IHR). Canonical transient receptor potential 3 (TRPC3) channels are integral to the propagation of seizures in SE, and vascular smooth muscle cell (VSMC) TRPC3 channels participate in vasoconstriction. Therefore, we hypothesize that cerebrovascular TRPC3 channels may contribute to seizure-induced IHR. To examine this possibility, we developed a smooth muscle-specific TRPC3 knockout (TRPC3smcKO) mouse. To quantify changes in neurovascular coupling, we combined laser speckle contrast imaging with simultaneous electroencephalogram recordings. Control mice exhibited multiple IHRs, and a limited increase in cerebral blood flow during SE with a high degree of moment-to-moment variability in which blood flow was not correlated with neuronal activity. In contrast, TRPC3smcKO mice showed a greater increase in blood flow that was less variable and was positively correlated with neuronal activity. Genetic ablation of smooth muscle TRPC3 channels shortened the duration of SE by eliminating a secondary phase of intense seizures, which was evident in littermate controls. Our results are consistent with the idea that TRPC3 channels expressed by cerebral VSMCs contribute to the IHR during SE, which is a critical factor in the progression of SE.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Nature
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by/2.5/ar/
dc.subject
TRPC3
dc.subject.classification
Biología Celular, Microbiología
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
Vascular smooth muscle TRPC3 channels facilitate the inverse hemodynamic response during status epilepticus
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2021-09-27T15:24:57Z
dc.identifier.eissn
2045-2322
dc.journal.volume
10
dc.journal.number
1
dc.journal.pagination
1-10
dc.journal.pais
Reino Unido
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dc.description.fil
Fil: Cozart, Michael A.. University of Arkansas for Medical Sciences; Estados Unidos
dc.description.fil
Fil: Phelan, Kevin D.. University of Arkansas for Medical Sciences; Estados Unidos
dc.description.fil
Fil: Wu, Hong. University of Arkansas for Medical Sciences; Estados Unidos
dc.description.fil
Fil: Mu, Shengyu. University of Arkansas for Medical Sciences; Estados Unidos
dc.description.fil
Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina
dc.description.fil
Fil: Rusch, Nancy J.. University of Arkansas for Medical Sciences; Estados Unidos
dc.description.fil
Fil: Zheng, Fang. University of Arkansas for Medical Sciences; Estados Unidos
dc.journal.title
Scientific Reports
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1038/s41598-020-57733-0
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/s41598-020-57733-0
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