Glutamate-induced oxidative stress, but not cell death, is largely dependent upon extracellular calcium in mouse neuronal HT22 cells

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dc.contributor.authorJong Seong Ha-
dc.contributor.authorSung Sup Park-
dc.date.accessioned2017-04-19T09:03:59Z-
dc.date.available2017-04-19T09:03:59Z-
dc.date.issued2006-
dc.identifier.issn0304-3940-
dc.identifier.uri10.1016/j.neulet.2005.09.056ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7258-
dc.description.abstractElucidating the relationship of glutamate-induced Ca2+ flux and oxidative death of neuronal cells may be of great relevance for neurodegenerative diseases in human beings. Mouse hippocampal HT22 cells provide a model system to study this relationship at the molecular level. Here we show that stimulation of HT22 cells with 5 mM glutamate is cytotoxic. Glutamate-induced cytotoxicity was associated with the generation of reactive oxygen species (ROS) and activation of the death executioner caspases 1 and 3. Treatment of HT22 cells with the calcium chelator, EGTA, and the calcium channel blocker, CoCl2, revealed that glutamate-induced cell death was dependent, in part, on glutamate-induced Ca2+ influx from extracellular stores. However, activation of caspases 1 and 3 and death of HT22 cells were also observed when Ca2+ was lacking in the extracellular milieu and ROS production abrogated. These findings led us to conclude that glutamate-induced death of mouse HT22 cells utilizes a complex mechanism that relies only in part on Ca2+ influx and ROS production. Additional studies are warranted to evaluate glutamate-induced death mechanisms that operate independently of Ca2+ influx and generation of ROS.-
dc.publisherElsevier-
dc.titleGlutamate-induced oxidative stress, but not cell death, is largely dependent upon extracellular calcium in mouse neuronal HT22 cells-
dc.title.alternativeGlutamate-induced oxidative stress, but not cell death, is largely dependent upon extracellular calcium in mouse neuronal HT22 cells-
dc.typeArticle-
dc.citation.titleNeuroscience Letters-
dc.citation.number2-
dc.citation.endPage169-
dc.citation.startPage165-
dc.citation.volume393-
dc.contributor.affiliatedAuthorJong Seong Ha-
dc.contributor.affiliatedAuthorSung Sup Park-
dc.contributor.alternativeName하종성-
dc.contributor.alternativeName박성섭-
dc.identifier.bibliographicCitationNeuroscience Letters, vol. 393, no. 2, pp. 165-169-
dc.identifier.doi10.1016/j.neulet.2005.09.056-
dc.subject.keywordCa2+-
dc.subject.keywordExcitotoxicity-
dc.subject.keywordGlutamate-
dc.subject.keywordReactive oxygen species-
dc.subject.localCa2+-
dc.subject.localExcitotoxicity-
dc.subject.localexcitotoxicity-
dc.subject.localGlutamate-
dc.subject.localglutamate-
dc.subject.localReactive oxidative species-
dc.subject.localReactive oxygen species(ROS)-
dc.subject.localReactive oxygen species-
dc.subject.localReactive Oxygen Species (ROS)-
dc.subject.localReactive Oxygen Species-
dc.subject.localROS-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localreactive oxygen species-
dc.subject.localreactive oxygen species (ROS)-
dc.description.journalClassY-
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Aging Convergence Research Center > 1. Journal Articles
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