ALTERED MATURATION OF BRAIN MITOCHONDRIA BY POSTNATAL HYPOXIA AND HIGH ALTITUDE IN LABORATORY RATS AND MICE.

Abstract

Living at high altitudes (HA) requires profound tuning of cellular metabolism to maintain homeostasis. Postnatal development at HA results in slower growth rates and modifications in homeostatic functions. While oxygen utilization is optimized in species adapted to HA, the metabolic plasticity during postnatal development remains unknown. This study uses a divergent adaptation model to HA in FVB mice and SD rats to evaluate mitochondrial oxygen consumption rates (OCR) in the retrosplenial cortex.