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Roles of glutamate in brain injuries after subarachnoid hemorrhage

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dc.contributor.authorKawakita, Fumihiro
dc.contributor.authorKanamaru, Hideki
dc.contributor.authorAsada, Reona
dc.contributor.authorSuzuki, Yume
dc.contributor.authorNampei, Mai
dc.contributor.authorNakajima, Hideki
dc.contributor.authorOinaka, Hiroki
dc.contributor.authorSuzuki, Hidenori
dc.date.accessioned2023-03-07T08:47:17Z
dc.date.available2023-03-07T08:47:17Z
dc.date.issued2022
dc.description.abstractAneurysmal subarachnoid hemorrhage (SAH) is a stroke type with a high rate of mortality and morbidity. Post-SAH brain injury as a determinant of poor outcome is classified into the following two types: early brain injury (EBI) and delayed cerebral ischemia (DCI). EBI consists of various acute brain pathophysiologies that occur within the first 72 hours of SAH in a clinical setting. The underlying mechanisms of DCI are considered to be cerebral vasospasm or microcirculatory disturbance, which develops mostly 4 to 14 days after clinical SAH. Glutamate is the principal neurotransmitter in the central nervous system, but excessive glutamate is known to induce neurotoxicity. Experimental and clinical studies have revealed that excessive glutamates are released after SAH. In addition, many studies have reported the relationships between excessive glutamate release or overactivation of glutamate receptors and excitotoxicity, cortical spreading depolarization, seizure, increased blood-brain barrier permeability, neuroinflammation, microthrombosis formation, microvasospasm, cerebral vasospasm, impairments of brain metabolic supply and demand, impaired neurovascular coupling, and so on, all of which potentially contribute to the development of EBI or DCI. As glutamates always exert their functions through one or more of 4 major receptors of glutamates, it would be valuable to know the mechanisms as to how glutamates cause these pathologies, and the possibility that a glutamate receptor antagonist may block the pathologies. To prevent the mechanistic steps leading to glutamatemediated neurotoxicity may ameliorate SAH-induced brain injuries and improve the outcomes. This review addresses the current knowledge of glutamate-mediated neurotoxicity, focusing on EBI and DCI after SAH.es
dc.formatapplication/pdfes
dc.format.extent11es
dc.identifier.doihttps://doi.org/10.14670/HH-18-509
dc.identifier.eisbnHistology and Histopathology Vol. 37, nº11 (2022)es
dc.identifier.issn0213-3911
dc.identifier.issn1699-5848
dc.identifier.urihttp://hdl.handle.net/10201/129123
dc.languageenges
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histiologiaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectCerebral vasospasmes
dc.subjectCortical spreading depolarizationes
dc.subjectDelayed cerebral ischemiaes
dc.subjectEarly brain injuryes
dc.subjectGlutamatees
dc.subjectNeurovascular couplinges
dc.subjectSubarachnoid hemorrhagees
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleRoles of glutamate in brain injuries after subarachnoid hemorrhagees
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.37,nº11 (2022)