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Excitotoxicity is required for induction of oxidative stress and apoptosis in mouse striatum by the mitochondrial toxin, 3-nitropropionic acid.

Authors
 Gyung W. Kim  ;  Jean-Christophe copin  ;  Makoto Kawase  ;  Sylvia F. Chen  ;  Shuzo Sato  ;  Glenn T. Gobbel  ;  Pak H. Chan 
Citation
 Journal of Cerebral Blood Flow and Metabolism, Vol.20(1) : 119-129, 2000 
Journal Title
 Journal of Cerebral Blood Flow and Metabolism 
ISSN
 0271-678X 
Issue Date
2000
MeSH
Animals ; Apoptosis/physiology* ; Caspases/metabolism ; Corpus Striatum/metabolism ; Corpus Striatum/pathology ; Corpus Striatum/physiopathology* ; Decerebrate State/metabolism ; Dizocilpine Maleate/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology ; Female ; In Situ Nick-End Labeling ; Mice ; Mice, Inbred C57BL ; Mitochondria/drug effects ; Nervous System/drug effects ; Nervous System/physiopathology ; Neurotoxins/metabolism* ; Nitro Compounds ; Oxidative Stress/physiology* ; Propionates/pharmacology* ; Propionates/poisoning ; Quinoxalines/pharmacology ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors ; Superoxides/metabolism
Keywords
3-Nitropropionic acid ; Striatum ; Mitochondria ; Excitotoxicity ; Superoxide ; Apoptosis
Abstract
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.
Full Text
http://journals.sagepub.com/doi/abs/10.1097/00004647-200001000-00016
DOI
10.1097/00004647-200001000-00016
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Gyung Whan(김경환) ORCID logo https://orcid.org/0000-0001-7053-4372
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/171683
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