Coenzyme Q10 supplementation improves the motor function of middle-aged mice by restoring the neuronal activity of the motor cortex
Ritsuko Inoue, Masami Miura, Shuichi Yanai, Hiroshi Nishimune
Abstract
Abstract Physiological aging causes motor function decline and anatomical and biochemical changes in the motor cortex. We confirmed that middle-aged mice at 15–18 months old show motor function decline, which can be restored to the young adult level by supplementing with mitochondrial electron transporter coenzyme Q 10 (CoQ 10 ) as a water-soluble nanoformula by drinking water for 1 week. CoQ 10 supplementation concurrently improved brain mitochondrial respiration but not muscle strength. Notably, we identified an age-related decline in field excitatory postsynaptic potential (fEPSP) amplitude in the pathway from layers II/III to V of the primary motor area of middle-aged mice, which was restored to the young adult level by supplementing with CoQ 10 for 1 week but not by administering CoQ 10 acutely to brain slices. Interestingly, CoQ 10 with high-frequency stimulation induced NMDA receptor-dependent long-term potentiation (LTP) in layer V of the primary motor cortex of middle-aged mice. Importantly, the fEPSP amplitude showed a larger input‒output relationship after CoQ 10 -dependent LTP expression. These data suggest that CoQ 10 restores the motor function of middle-aged mice by improving brain mitochondrial function and the basal fEPSP level of the motor cortex, potentially by enhancing synaptic plasticity efficacy. Thus, CoQ 10 supplementation may ameliorate the age-related decline in motor function in humans.