At a dose of 20 mg/kg, it reduced depression-like behavior in the FST and SPT, reduced the increase in plasma ACTH and corticosterone levels, normalized levels of serotonin and norepinephrine in the hippocampus and prefrontal cortex, and induced the hippocampal production of BDNF and its receptor, tropomyosin-related kinase B (TrkB), by activating the ERK signaling pathway [220]. This evidence concerns the gene BDNF and depressive symptom measurement.