Apoptotic cell death in vulnerable subpopulation of cerebellar granule cells

1997 ◽  
Vol 94 (5) ◽  
pp. 517-518 ◽  
Author(s):  
A. Hara ◽  
Masayuki Niwa ◽  
Naoki Yoshimi ◽  
Hideki Mori
Keyword(s):  
Cell Death ◽  
Granule Cells ◽  
Cerebellar Granule Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cerebellar Granule

Apoptotic cell death of cerebellar granule cells in rolling mouse Nagoya

2002 ◽  
Vol 325 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Young Suk Suh ◽  
Sen-ich Oda ◽  
Yoon Hee Kang ◽  
Hyun Kim ◽  
Im Joo Rhyu
Keyword(s):  
Cell Death ◽  
Granule Cells ◽  
Cerebellar Granule Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cerebellar Granule

Paraquat-induced apoptotic cell death in cerebellar granule cells

2004 ◽  
Vol 1011 (2) ◽  
pp. 170-176 ◽  
Author(s):  
Rosa A González-Polo ◽  
Andrea Rodrı́guez-Martı́n ◽  
José M Morán ◽  
Mireia Niso ◽  
Germán Soler ◽  
...  
Keyword(s):  
Cell Death ◽  
Granule Cells ◽  
Cerebellar Granule Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cerebellar Granule

Rat cerebellar granule cells are protected from glutamate-induced excitotoxicity by S-nitrosoglutathione but not glutathione

2004 ◽  
Vol 286 (4) ◽  
pp. C893-C904 ◽  
Author(s):  
Chung-Yu Li ◽  
Ting-Yu Chin ◽  
Sheau-Huei Chueh
Keyword(s):  
Cell Death ◽  
Glial Cells ◽  
Granule Cells ◽  
Cerebellar Granule Cells ◽  
Apoptotic Cell ◽  
Ros Generation ◽  
No Donor ◽  
No Donors ◽  
Cerebellar Granule ◽  
Ros Scavenger

In cultured rat cerebellar granule cells, glutamate or N-methyl-d-aspartate (NMDA) activation of the NMDA receptor caused a sustained increase in cytosolic Ca2+ levels ([Ca2+]i), reactive oxygen species (ROS) generation, and cell death (respective EC50 values for glutamate were 12, 30, and 38 μM) but no increase in caspase-3 activity. Removal of extracellular Ca2+ blocked all three glutamate-induced effects, whereas pretreatment with an ROS scavenger inhibited glutamate-induced cell death but had no effect on the [Ca2+]i increase. This indicates that glutamate-induced cell death is attributable to [Ca2+]i increase and ROS generation, and the [Ca2+]i increase precedes ROS generation. Apoptotic cell death was not seen until 24 h after exposure of cells to glutamate. S-nitrosoglutathione abolished glutamate-induced ROS generation and cell death, and only a transient [Ca2+]i increase was seen; similar results were observed with another nitric oxide (NO) donor, S-nitroso- N-acetylpenicillamine, but not with glutathione, which suggests that the effects were caused by NO. The transient [Ca2+]i increase and the abolishment of ROS generation induced by glutamate and S-nitrosoglutathione were still seen in the presence of an ROS scavenger. Glial cells, which were present in the cultures used, showed no [Ca2+]i increase in the presence of glutamate, and glutamate-induced granule cell death was independent of the percentage of glial cells. In conclusion, NO donors protect cultured cerebellar granule cells from glutamate-induced cell death, which is mediated by ROS generated by a sustained [Ca2+]i increase, and glial cells provide negligible protection against glutamate-induced excitotoxicity.

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