Journal of pain research · 2026
Transcranial Direct Current Stimulation Targeting the Primary Motor Cortex Suppresses Activity in the Ventrolateral Periaqueductal Gray and Alleviates Chronic Pain in a Rat Model of Knee Osteoarthritis.
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Xu Yifan, Fan Chenglei, Xue Junqiang, Gao Chengfei, Zhou Yu, Li Tieshan
Аннотация
PURPOSE: Transcranial direct current stimulation (tDCS) shows promise for chronic pain treatment; however, its efficacy and mechanisms in knee osteoarthritis (KOA)-associated pain remain unclear. This study aimed to evaluate the analgesic effects of primary motor cortex (M1)-targeted tDCS in a rat model of KOA and to investigate the underlying mechanisms.
METHODS: A chronic KOA model was established via unilateral intra-articular monoiodoacetate (MIA) injection. Mechanical allodynia and thermal hyperalgesia were assessed using von Frey filaments and a hot plate test. Neuronal activation and microglial responses in the ventrolateral periaqueductal gray (vlPAG) were evaluated by immunohistochemistry, and inflammatory cytokines were quantified using qPCR. The effects of M1-targeted tDCS on vlPAGactivity, microglial activation, and pain behaviors were examined. Minocycline was administered into the vlPAG to inhibit microglial. CTB-555 retrograde tracing was used to map M1-vlPAG connectivity.
RESULTS: MIA induced persistent pain hypersensitivity, accompanied by increased neuronal activity, microglial activation, and elevated pro-inflammatory cytokines in the contralateral vlPAG. Local administration of minocycline suppressed both microglial and neuronal activation and alleviated pain behaviors. M1-targeted tDCS significantly reduced pain hypersensitivity, suppressed vlPAG neuronal activity and microglial activation, and downregulated inflammatory cytokines expression.
CONCLUSION: KOA-associated chronic pain is linked to increased neuronal activity and neuroinflammation in the vIPAG. M1-targeted tDCS alleviates pain, likely by suppressing vIPAG activity and microglial-mediated inflammation via the M1-vlPAG pathway. However, given differences between the MIA model and human osteoarthritis, caution is required in clinical translation.
METHODS: A chronic KOA model was established via unilateral intra-articular monoiodoacetate (MIA) injection. Mechanical allodynia and thermal hyperalgesia were assessed using von Frey filaments and a hot plate test. Neuronal activation and microglial responses in the ventrolateral periaqueductal gray (vlPAG) were evaluated by immunohistochemistry, and inflammatory cytokines were quantified using qPCR. The effects of M1-targeted tDCS on vlPAGactivity, microglial activation, and pain behaviors were examined. Minocycline was administered into the vlPAG to inhibit microglial. CTB-555 retrograde tracing was used to map M1-vlPAG connectivity.
RESULTS: MIA induced persistent pain hypersensitivity, accompanied by increased neuronal activity, microglial activation, and elevated pro-inflammatory cytokines in the contralateral vlPAG. Local administration of minocycline suppressed both microglial and neuronal activation and alleviated pain behaviors. M1-targeted tDCS significantly reduced pain hypersensitivity, suppressed vlPAG neuronal activity and microglial activation, and downregulated inflammatory cytokines expression.
CONCLUSION: KOA-associated chronic pain is linked to increased neuronal activity and neuroinflammation in the vIPAG. M1-targeted tDCS alleviates pain, likely by suppressing vIPAG activity and microglial-mediated inflammation via the M1-vlPAG pathway. However, given differences between the MIA model and human osteoarthritis, caution is required in clinical translation.