Chemogenetics Modulation of Electroacupuncture Analgesia in Mice Spared Nerve Injury-Induced Neuropathic Pain through TRPV1 Signaling Pathway

Neuropathic pain, resulting from somatosensory cortex malfunction, causes inflammation and activates glial cells, leading to neuroinflammation. Electroacupuncture (EA) has shown promise in treating neuropathic pain by reducing inflammation and affecting the TRPV1 signaling pathway. A novel chemogenetics method was used to precisely inhibit SSC to ACC activity, which showed an analgesic effect through the TRPV1 pathway.

• 1
  Electroacupuncture (EA) at 2 Hz partially attenuated mechanical hyperalgesia and fully reduced thermal hyperalgesia in mice with spared nerve injury (SNI).
• 2
  Mice with Trpv1 deletion showed partial mechanical hyperalgesia and no significant thermal hyperalgesia induction in neuropathic pain.
• 3
  EA treatment and Trpv1 deletion reduced levels of inflammatory factors, such as interleukin-1 beta (IL1-β), IL-3, IL-6, IL-12, IL-17, tumor necrosis factor alpha, and interferon gamma, elevated by SNI modeling.