• A S Aguiar, E Stragier, D da Luz Scheffer, A P Remor, P A Oliveira, R D Prediger, A Latini, R Raisman-Vozari, R Mongeau, and L Lanfumey.
• Departamento de Bioquímica, Universidade Federal de Santa Catarina, UFSC, Centro de Ciências Biológicas, CCB, Florianópolis, SC 88049-900, Brazil; Departamento de Farmacologia, Universidade Federal de Santa Catarina, UFSC, Centro de Ciências Biológicas, CCB, Florianópolis, SC 88049-900, Brazil. Electronic address: aderbalaguiar@gmail.com.
• Neuroscience. 2014 Jun 20;271:56-63.

AbstractThe present study was aimed at analyzing the effects of physical exercise on mitochondrial physiology, anxio-depressive-like behaviors and neuroplasticity in mice. Adult C57BL/6J male mice were isolated in home cages equipped or not with free-running wheels. After 6weeks of exercise, mice were tested in various behavioral paradigms to evaluate anxiety- and depressive-like behaviors. The hippocampi were dissected for neurochemical assays, including mitochondrial activity, monoamines content and the expression of genes involved in energy metabolism and brain-derived neurotrophic factor (BDNF) regulation. Exercise decreased anxiety-like behaviors in the open field and elevated plus maze, and exerted antidepressant-like effects in the tail suspension test. Exercise stimulated brain mitochondrial activity and increased resistance against rotenone, an inhibitor of complex I activity. Furthermore, mRNA expression of Bdnf, Gdnf, Tfam (mitochondrial transcription factor A), and Ndufa6 (mitochondrial I subunit) genes, as well as the phosphorylation of cAMP response element-binding protein were increased after exercise. In summary, exercise appears to engage mitochondrial pathways and to potentiate neuroplasticity and might be associated to mood improvement.Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

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