Nitric oxide synthase and mitochondrial function in hippocampus and cerebral cortex of rats exposed to enriched environments.

LORES-ARNAIZ, S.; BUSTAMANTE, J.; CZERNICZYNIEC, A.; KARAK, M.; LORES ARNAIZ, M.R.

Montevideo, Uruguay

Congreso; V Meeting of SFRBM – South American Group, V International Conference on Peroxynitrite and Reactive Nitrogen Species.; 2007

Society for Free Radical Biology and Medicine

Nitric oxide (NO) has been postulated as neuronal messenger in experimental models of synaptic plasticity. Previous results from this laboratory have shown that exposition to enriched environments (EE), prevents the aging impairment of spatial cognition through NO-dependent mechanisms. In this study we evaluated the effect of EE exposure on mitochondrial function and on nitric oxide synthase (NOS) in hippocampus and cerebral cortex. Male rats (21 days) were assigned to EE or to standard environment (SE) for 1 year. Oxygen consumption, mitochondrial permeability transition (MPT), and mitochondrial membrane potential (Dj) were determined in hippocampal and cerebral cortex mitochondria. NOS activity and expression were assayed in submitochondrial membranes. State 3 respiratory rate was increased by 80% in cerebral cortex mitochondria from EE rats; no changes were observed in hippocampal mitochondria after EE exposure. Calcium induced-MPT was 40% and 53% lower in hippocampal and cerebral cortex mitochondria from EE rats, as compared with SE rats. Calcium loading induced membrane depolarization in hippocampal and cerebral cortex mitochondria from SE animals but only induced slight changes in mitochondrial Dj in EE rats. NOS activity was increased by 195% in cerebral cortex mitochondria but decreased by 47% in hippocampal mitochondria from EE rats, as compared with SE rats. Western blot analysis revealed a similar pattern of nNOS protein expression. Our results suggest that both in hippocampus and cerebral cortex, EE exposition allows the maintainance of mitochondrial permeability and membrane potential, assuring continuous energy supply. In cerebral cortex, but not in hippocampus, improvement in mitochondrial function seems to be associated with increased NO production.