Generally, in rat models of depression, EA can inhibit excessive excitement of the HPA axis, reduce inflammatory cytokine levels, improve the expression of brain-derived neurotrophic factor (BDNF), restore hippocampal synaptic plasticity, induce bidirectional regulation of neuropeptides and neurotransmitters, and induce signal transduction pathways and genome expression to exert a beneficial effect in the treatment of depression. The gene discussed is BDNF; the disease is depressive symptom measurement.