Chronic stress induces the expression of inducible nitric oxide synthase in rat brain cortex.

摘要: Long-term exposure to stress has detrimental effects on several brain functions in many species, including humans, and leads neurodegenerative changes. However, the underlying neural mechanisms by which causes neurodegeneration are still unknown. We have investigated role of endogenously released nitric oxide (NO) this phenomenon possible induction inducible NO synthase (iNOS) isoform. In adult male rats, (immobilization for 6 h during 21 days) increases activity a calcium-independent induces expression iNOS cortical neurons as seen immunohistochemical western blot analysis. Three weeks repeated immobilization immunoreactivity nitrotyrosine, nitration product peroxynitrite. Repeated accumulation metabolites NO2+ NO3- (NOx-) cortex, these changes occur parallel with lactate dehydrogenase (LDH) release impairment glutamate uptake synaptosomes. Administration selective inhibitor aminoguanidine (400 mg/kg i.p. daily from days 7 stress) prevents NOx- LDH release, Taken together, findings indicate that sustained overproduction via may be responsible, at least part, some caused support neuroprotective specific inhibitors situation.