Chronic Cerebral Hypoperfusion Induces Striatal Alterations Due to the Transient Increase of NO Production and the Depression of Glutathione Content View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2002-04

AUTHORS

Ken-ichi Tanaka, Naoko Wada-Tanaka, Ikuko Miyazaki, Masahiko Nomura, Norio Ogawa

ABSTRACT

We examined the effects of chronic cerebral hypoperfusion on the endogenous oxidative stress-related indices, nitrite and nitrate (NOx) concentration, glutathione (GSH) content, superoxide dismutase and catalase activities, and thiobarbituric acid-reactive substances level in the rat striatum, to clarify the participation of oxidative stress in the chronic cerebral hypoperfusion-induced alterations. Our present results indicate that chronic cerebral hypoperfusion produces oxidative stress and disturbs intracellular redox regulation in two distinct phases: at 1 day, "acute" and at 6 weeks, "chronic" alterations after the operation. Therefore, striatal neural cell damage may be mainly attributed to the transient increase of NOx production at 1 day after, and the delayed reduction of muscarinic acetylcholine receptor binding in the striatum may be mostly attributed to the continuous depression of GSH content from the 1st to the 6th postoperative week. In particular, the continuous GSH depression may be considered to accompany the pathophysiology of chronic cerebral hypoperfusion. More... »

PAGES

331-336

Identifiers

URI

http://scigraph.springernature.com/pub.10.1023/a:1014967414468

DOI

http://dx.doi.org/10.1023/a:1014967414468

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1014066284

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11958536


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