Pain is associated with several conditions, such as
inflammation, that result from altered peripheral nerve properties.
Electroacupuncture (EA) is a common Chinese clinical medical technology used for
pain management. Using an inflammatory
pain mouse model, we investigated the effects of EA on the regulation of neurons, microglia, and related molecules. Complete
Freund's adjuvant (CFA)
injections produced a significant mechanical and
thermal hyperalgesia that was reversed by EA or a transient receptor potential V1 (TRPV1) gene deletion. The expression of the astrocytic marker
glial fibrillary acidic protein (GFAP), the microglial marker Iba-1, S100B,
receptor for advanced glycation end-products (RAGE), TRPV1, and other related molecules was dramatically increased in the dorsal root ganglion (DRG) and spinal cord dorsal horn (SCDH) of CFA-treated mice. This effect was reversed by EA and TRPV1 gene deletion. In addition, endomorphin (EM) and
N6-cyclopentyladenosine (CPA) administration reliably reduced mechanical and
thermal hyperalgesia, thereby suggesting the involvement of
opioid and
adenosine receptors. Furthermore, blocking of
opioid and
adenosine A1 receptors reversed the
analgesic effects of EA. Our study illustrates the substantial
therapeutic effects of EA against inflammatory
pain and provides a novel and detailed mechanism underlying EA-mediated
analgesia via neuronal and non-neuronal pathways.