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Effect of Electroacupuncture at Fengchi on Facial Allodynia, Microglial Activation, and Microglia–Neuron Interaction in a Rat Model of Migraine
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Effect of Electroacupuncture at Fengchi on Facial Allodynia, Microglial Activation, and Microglia–Neuron Interaction in a Rat Model of Migraine
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Effect of Electroacupuncture at Fengchi on Facial Allodynia, Microglial Activation, and Microglia–Neuron Interaction in a Rat Model of Migraine
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Journal Article
Effect of Electroacupuncture at Fengchi on Facial Allodynia, Microglial Activation, and Microglia–Neuron Interaction in a Rat Model of Migraine
2022
Overview
The purpose of the work was to investigate whether electroacupuncture (EA) could ameliorate migraine central sensitization by modulating microglial activation and the subsequent release of inflammatory cytokines in the trigeminal nucleus caudalis (TNC) in a rat model. Establishment of a rat model of recurrent migraine was achieved through repeated dural electrical stimulation (DES). After nine sessions of acupuncture treatment at Fengchi (GB20), facial mechanical thresholds were measured by electronic von Frey measurements. Microglial activation and cytokine receptors of TNC were evaluated by immunofluorescence staining. The expression of microglial biological marker Ibal-1, proinflammatory cytokines, and cytokine receptors in the TNC were evaluated by Western blot and/or real-time polymerase chain reaction. In addition, the effects of inhibition of microglial activation on facial thresholds and neuronal activation (i.e., expression of c-Fos in the TNC) induced by DES were observed. After consecutive EA-GB20 treatments, the facial withdrawal threshold was significantly higher than in the model group at different time points (p < 0.05). The hyperreactivity of microglia induced by DES was significantly inhibited, and the expressions of Ibal-1, interleukin-1β, tumor necrosis factor-α, and their receptors in the TNC were also significantly decreased (p < 0.05). Inhibition of microglia by minocycline demonstrated an acupuncture-like role, which was manifested by ameliorated mechanical hyperalgesia and decreased neuronal expression of c-Fos, Iba-1, and inflammatory factors. EA at GB20 could ameliorate migraine facial allodynia by inhibiting microglial activation and the subsequent release of inflammatory cytokines and their receptors in the TNC.
