상세 정보

underline
Metadata Downloads : dc(xml) or Excel
Cited 0 time in scopus ci

Title 

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

Authors 

Jong Seong HaSung Sup Park

Publisher 

Elsevier

Issue Date 

2006

Citation 

Neuroscience Letters, vol. 393, no. 2, pp. 165-169

Keywords 

Ca2+excitotoxicityglutamatereactive oxygen speciescalciumcalcium channel blocking agentcalcium chelating agentanimal cellcalcium transportcell death

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.

ISSN 

0304-3940

Link 

http://dx.doi.org/10.1016/j.neulet.2005.09.056

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


There are no files associated with this item.
qrcode

FusionCharts.
DSpace Software Coptright(c) 2010 MIT and Hewleft-Packard  /  KRIBB-REPOSITORY ( Email:jakim@kribb.re.kr)