In conclusion, although stress causes derangement of brain monoamine metabolism and monoaminergic neurotransmission [1], pharmacological pre-treatments and exercise, which induce long-lasting adaptations in several monoaminergic systems [15, 47, 54], could effectively prevent the stress-induced anxiety- and depression-like behaviors and memory impairment, the latter of which could be explained by hippocampal BDNF protein expression. This evidence concerns the gene BDNF and depressive symptom measurement.