Using the data previously described as our basis, we suggest that the potential of magnesium to enhance the BDNF level in OB rats and the differentiated effects on AMPARs in the hippocampus and the PFC may be the primary mechanisms responsible for the effectiveness of magnesium in depression animal models, i.e., the OB model, as well as anxiety animal models. The gene discussed is BDNF; the disease is depressive symptom measurement.