INVESTIGADORES
LORES ARNAIZ Silvia
congresos y reuniones científicas
Título:
Nitric oxide synthase and mitochondrial function in hippocampus and cerebral cortex of rats exposed to enriched environments.
Autor/es:
LORES-ARNAIZ, S.; BUSTAMANTE, J.; CZERNICZYNIEC, A.; CUELLO, M.; LORES ARNAIZ, M.R.
Lugar:
Montevideo
Reunión:
Congreso; V Meeting of SFRBM South American Group, V International Conference on Peroxynitrite and Reactive Nitrogen Species.; 2007
Resumen:
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.