Exercise during adolescence attenuated depressive-like behaviors and hippocampal mitochondrial dysfunction following early life stress in adult male rats

Fattahi Masrour, Forouzan; Peeri, Maghsoud; Hosseini, Mir-Jamal; Azarbayjani, Mohammad Ali

doi:10.22037/ijpr.2018.2372

Exercise during adolescence attenuated depressive-like behaviors and hippocampal mitochondrial dysfunction following early life stress in adult male rats

Document Type: Research article

Authors

¹ Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran.

² Zanjan Applied Pharmacology Research Center, Zanjan University of Medical sciences, Zanjan, Iran.

³ Department of exercise physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran.

10.22037/ijpr.2018.2372

Abstract

Purpose: In this study, we assumed that treating animals with an antidepressant agents or voluntary running wheel exercise (RW) during adolescence may have protective effects against early life stress (ELS) which can impact on behavior and mitochondrial function. Evidence indicates that ELS has deleterious effects on brain and behavior and increases the risk of mental disorders such as depression. Methods: Maternal separation stress (MS) model to male rats (postnatal day or PND2-PND14) were performed to determination of depressive-like behaviors using the forced swimming test, splash test and mitochondrial function in the hippocampus. Results: Treating MS rats with both RW and fluoxetine (5 mg/kg/day, i.p) during adolescence (PND30-PND60) produced antidepressant-like effects in animals and attenuated the negative effects of ELS on hippocampal mitochondrial function in adult male rats. The results of present study showed that (non) pharmacological treatments during adolescence are able to produce protective effects against long-lasting effects of ELS on behavior and mitochondrial function. Conclusion: These results highlighted the importance of adolescence as an important stage of life and the long-lasting effects of ELS on hippocampal mitochondrial function which can suggest the possible involvement of abnormal mitochondrial function in pathophysiology of depression following experiencing ELS.

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