The mechanisms of neuronal death produced by mitochondrial toxin 3-nitropropionic acid: the roles of N-methyl-D-aspartate glutamate receptors and mitochondrial calcium overload

Neuroscience ◽  
2002 ◽  
Vol 112 (3) ◽  
pp. 707-716 ◽  
Author(s):  
W.T Lee ◽  
H.S Yin ◽  
Y.Z Shen
Keyword(s):  
Glutamate Receptors ◽  
Neuronal Death ◽  
Calcium Overload ◽  
Mitochondrial Calcium ◽  
Nitropropionic Acid ◽  
Mitochondrial Toxin ◽  
3 Nitropropionic Acid

scholarly journals Excitotoxicity is Required for Induction of Oxidative Stress and Apoptosis in Mouse Striatum by the Mitochondrial Toxin, 3-Nitropropionic Acid

2000 ◽  
Vol 20 (1) ◽  
pp. 119-129 ◽  
Author(s):  
Gyung W. Kim ◽  
Jean-Christophe Copin ◽  
Makoto Kawase ◽  
Sylvia F. Chen ◽  
Shuzo Sato ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Neuronal Death ◽  
Nmda Receptor Antagonist ◽  
Apoptosis Induction ◽  
Nitropropionic Acid ◽  
Mitochondrial Toxin ◽  
Apoptotic Neuronal Death ◽  
3 Nitropropionic Acid

Excitotoxicity is implicated in the pathogenesis of several neurologic diseases, such as chronic neurodegenerative diseases and stroke. Recently, it was reported that excitotoxicity has a relationship to apoptotic neuronal death, and that the mitochondrial toxin, 3-nitropropionic acid (3-NP), could induce apoptosis in the striatum. Although striatal lesions produced by 3-NP could develop through an excitotoxic mechanism, the exact relationship between apoptosis induction and excitotoxicity after 3-NP treatment is still not clear. The authors investigated the role of excitotoxicity and oxidative stress on apoptosis induction within the striatum after intraperitoneal injection of 3-NP. The authors demonstrated that removal of the corticostriatal glutamate pathway reduced superoxide production and apoptosis induction in the denervated striatum of decorticated mice after 3-NP treatment. Also, the N-methyl-d-aspartate (NMDA) receptor antagonist, MK-801, prevented apoptosis in the striatum after 3-NP treatment for 5 days, whereas the non-NMDA receptor antagonist, 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo(F)quinoxaline, was ineffective. The authors also evaluated the initial type of neuronal death by 3-NP treatment for different durations from 1 to 5 days. In early striatal damage, apoptotic neuronal death initially occurred after 3-NP treatment. Our data show that excitotoxicity related to oxidative stress initially induces apoptotic neuronal death in mouse striatum after treatment with 3-NP.

1311 Striatal astrocytic cell death following systemic administration of mitochondrial toxin, 3-nitropropionic acid

1996 ◽  
Vol 25 ◽  
pp. S144
Author(s):  
Hitoo Nishino ◽  
Atsuo Fukuda ◽  
Ichiro Fujimoto ◽  
Yasunobu Shimano ◽  
Hideki Hida
Keyword(s):  
Cell Death ◽  
Systemic Administration ◽  
Nitropropionic Acid ◽  
Mitochondrial Toxin ◽  
3 Nitropropionic Acid

Age-Dependent Vulnerability of the Striatum to the Mitochondrial Toxin 3-Nitropropionic Acid

1993 ◽  
Vol 60 (1) ◽  
pp. 356-359 ◽  
Author(s):  
Emmanuel Brouillet ◽  
Bruce G. Jenkins ◽  
Bradley T. Hyman ◽  
Robert J. Ferrante ◽  
Neil W. Kowall ◽  
...  
Keyword(s):  
Nitropropionic Acid ◽  
Age Dependent ◽  
Mitochondrial Toxin ◽  
3 Nitropropionic Acid
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