therapeutic effects in premortem human brain tissue, many studies were also conducted on animals using approved animal models of depression. In their study, Huang and colleagues (2012) used three different paradigms to demonstrate the effects of exercise on behavior. In all three models, both rats that exercised daily and rats that were chronically treated with fluoxetine displayed less depressive-like patterns of behaviors compared to other conditions (enriched environment) or drugs (Clozapine, Haloperidol). Similarly, the biological effects induced by exercise in rats closely matched those induced by fluoxetine. Indeed, both exercise and fluoxetine acted by increasing neurogenesis and spinal density in the CA1 field of the hippocampus, a finding that was not shared by the rats in the other groups. Exercise was also found to increase levels of ß-endorphins, VEGF, BDNF as well as serotonin, and ultimately, to an increase in neurogenesis. This increase in cell proliferation may have been mediated by the increase in BDNF (Eisch, 2002). However, another study by Bjornebekk, Mather and Brene (2005) suggested that exercise increases cell proliferation independently of the levels of BDNF, as the latter, in contrast to cell proliferation, did not correlate with exercise’s antidepressant effect. Conclusion In conclusion, different treatment modalities for treating major depressive disorder, and most represent efficient ways of alleviating and even suppressing symptoms associated with depression. Although little is known about their underlying mechanism of action, they all seem to influence the rate of neurogenesis in the adult hippocampus, and the delayed onset of their therapeutic effects is a close match to the time needed for neuronal maturation (4 weeks). Additionally, reduction of symptoms is also associated
therapeutic effects in premortem human brain tissue, many studies were also conducted on animals using approved animal models of depression. In their study, Huang and colleagues (2012) used three different paradigms to demonstrate the effects of exercise on behavior. In all three models, both rats that exercised daily and rats that were chronically treated with fluoxetine displayed less depressive-like patterns of behaviors compared to other conditions (enriched environment) or drugs (Clozapine, Haloperidol). Similarly, the biological effects induced by exercise in rats closely matched those induced by fluoxetine. Indeed, both exercise and fluoxetine acted by increasing neurogenesis and spinal density in the CA1 field of the hippocampus, a finding that was not shared by the rats in the other groups. Exercise was also found to increase levels of ß-endorphins, VEGF, BDNF as well as serotonin, and ultimately, to an increase in neurogenesis. This increase in cell proliferation may have been mediated by the increase in BDNF (Eisch, 2002). However, another study by Bjornebekk, Mather and Brene (2005) suggested that exercise increases cell proliferation independently of the levels of BDNF, as the latter, in contrast to cell proliferation, did not correlate with exercise’s antidepressant effect. Conclusion In conclusion, different treatment modalities for treating major depressive disorder, and most represent efficient ways of alleviating and even suppressing symptoms associated with depression. Although little is known about their underlying mechanism of action, they all seem to influence the rate of neurogenesis in the adult hippocampus, and the delayed onset of their therapeutic effects is a close match to the time needed for neuronal maturation (4 weeks). Additionally, reduction of symptoms is also associated