Electroacupuncture (EA) stimulation at specific acupoints shows promise in alleviating depression by regulating key biochemical pathways, according to a 2025 review from researchers at Shanghai University of Traditional Chinese Medicine.
The study, conducted using a chronic unpredictable mild stress (CUMS) rat model of depression, found that EA applied to acupoints GV20 and Yintang (GV29, EX-HN3) significantly improved depressive-like behaviors over 14 days of daily treatment.
In the experiment, Sprague-Dawley rats underwent a validated CUMS protocol before receiving EA: 2 Hz low-frequency stimulation (0.6 mA) for 30 minutes daily via 0.25 mm × 25 mm filiform needles inserted 5 mm deep at the selected acupoints.
Behavioral assessments revealed notable improvements: rats showed increased sucrose consumption in the sucrose preference test (SPT), indicating reduced anhedonia, and enhanced locomotor activity in the open field test (OFT), suggesting alleviated psychomotor blockages—both core features of depressive states in rodent models.
Molecular analyses uncovered the biological mechanisms behind these effects. EA treatment upregulated the expression of brain-derived neurotrophic factor (BDNF) in the hippocampus, alongside increased levels of TrkB, BDNF’s high-affinity receptor.
It also boosted mRNA and protein levels of tissue-type plasminogen activator (tPA), an enzyme that converts inactive pro-BDNF to its bioactive form. These changes extended to the dorsal raphe nuclei, a brain region critical for serotonergic neurotransmission, highlighting EA’s role in modulating neurotrophic signaling across key brain areas linked to depression.
The chosen acupoints—GV20 and Yintang—lie on the Governing Vessel, a meridian traditionally used for central nervous system disorders.
The study’s low-frequency EA protocol stood out for its simplicity, reproducibility, and lack of pharmacologic agents, isolating EA as the sole therapeutic intervention. Notably, the two-week treatment produced rapid antidepressant effects, aligning with clinical feasibility.
These findings support EA as a non-pharmacological depression treatment that enhances endogenous neuroplasticity via BDNF-TrkB signaling—mirroring the biological targets of conventional antidepressants like SSRIs but without drug-related side effects.
The research strengthens the case for integrating EA into depression management, particularly for drug-nonresponsive patients or those preferring non-pharmacological options. Further human studies are needed, but the results provide a mechanistic foundation for EA’s antidepressant potential in evidence-based practice.
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