Possible mild exercise effects enhancing hippocampal plasticity : To develop an effective exercise regimen enhancing cognitive functions

Abstract

Chronic stress is the main risk factor in the development of depression and may cause hippocampal dysfunction resulting in memory deficits and HPS - axis hyperactivity. The reduction of adult hippocampal neurogenesis (AHN) and resultant hippocampal atrophy would also occur in patients with major depression. As a complementary therapy, stress - free mild exercise would be possible candidate, since even acute mild exercise below lactate threshold (LT) activates hippocampal neurons and its two weeks exercise training resulted in enhanced AHN, like antidepressant treatment and electroconvulsive therapy, which might be beneficial for depression. In our current study using rats, we found that 2 weeks of ME, that is defined below the LT enhanced AHN in mediating neurosteroid, dihydrotestosterone (DHT) , which is synthesized in hippocampus via de novo synthesis, and BDNF and IGF-Ⅰ may also be associated with its promoting AHN. Furthermore, in the six - week of mild exercise model that enhanced both AHN and spatial memory, we found that AHN are related to lipid metabolism (APOE) , protein synthesis (IGF2, IRS1) , and inflammatory response (IL1B, TNF) , known to be facilitatory factor for AHN. These results might serve in further elucidating the main pathway behind mild exercise - enhanced AHN and spatial memory. Collectively, it is tempting to conclude that even mild exercise, which is useful for anybody even vulnerable peoples, could have potential clinical impacts for depression, like depressants.