DC Field | Value | Language |
---|---|---|
dc.contributor.author | Jong Seong Ha | - |
dc.contributor.author | Sung Sup Park | - |
dc.date.accessioned | 2017-04-19T09:03:59Z | - |
dc.date.available | 2017-04-19T09:03:59Z | - |
dc.date.issued | 2006 | - |
dc.identifier.issn | 0304-3940 | - |
dc.identifier.uri | 10.1016/j.neulet.2005.09.056 | ko |
dc.identifier.uri | https://oak.kribb.re.kr/handle/201005/7258 | - |
dc.description.abstract | Elucidating 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.publisher | Elsevier | - |
dc.title | Glutamate-induced oxidative stress, but not cell death, is largely dependent upon extracellular calcium in mouse neuronal HT22 cells | - |
dc.title.alternative | Glutamate-induced oxidative stress, but not cell death, is largely dependent upon extracellular calcium in mouse neuronal HT22 cells | - |
dc.type | Article | - |
dc.citation.title | Neuroscience Letters | - |
dc.citation.number | 2 | - |
dc.citation.endPage | 169 | - |
dc.citation.startPage | 165 | - |
dc.citation.volume | 393 | - |
dc.contributor.affiliatedAuthor | Jong Seong Ha | - |
dc.contributor.affiliatedAuthor | Sung Sup Park | - |
dc.contributor.alternativeName | 하종성 | - |
dc.contributor.alternativeName | 박성섭 | - |
dc.identifier.bibliographicCitation | Neuroscience Letters, vol. 393, no. 2, pp. 165-169 | - |
dc.identifier.doi | 10.1016/j.neulet.2005.09.056 | - |
dc.subject.keyword | Ca2+ | - |
dc.subject.keyword | Excitotoxicity | - |
dc.subject.keyword | Glutamate | - |
dc.subject.keyword | Reactive oxygen species | - |
dc.subject.local | Ca2+ | - |
dc.subject.local | Excitotoxicity | - |
dc.subject.local | excitotoxicity | - |
dc.subject.local | Glutamate | - |
dc.subject.local | glutamate | - |
dc.subject.local | Reactive oxidative species | - |
dc.subject.local | Reactive oxygen species(ROS) | - |
dc.subject.local | Reactive oxygen species | - |
dc.subject.local | Reactive Oxygen Species (ROS) | - |
dc.subject.local | Reactive Oxygen Species | - |
dc.subject.local | ROS | - |
dc.subject.local | Reactive oxygen species (ROS) | - |
dc.subject.local | reactive oxygen species | - |
dc.subject.local | reactive oxygen species (ROS) | - |
dc.description.journalClass | Y | - |
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