Electroacupuncture may alleviate inflammatory pain by downregulating the expression of P2Y(14) receptor in the primary somatosensory cortex.

Increasing evidence indicated that purinergic signalling involved in electroacupuncture (EA)-induced analgesia. Whether purinergic P2Y(14) receptor contributes to EA-mediated analgesia remains unclear. Here, we report that the expression of P2Y(14) receptor in the hindlimb region of the primary somatosensory cortex (S1HL) was significantly upregulated on Complete Freund's Adjuvant (CFA)-induced pain model mice, while was downregulated after EA treatment (2 Hz frequency, 1 mA intensity, and 30 min duration) at "Zusanli" (also named ST36 acupoint). EA-mediated analgesia could be reversed by injection of P2RY(14) agonist uridine diphosphate glucose (UDPG) into the bilateral S1HL, while prolonged by injection of P2RY(14) antagonist pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid (PPTN). It suggested that EA may alleviate inflammatory pain by downregulating the expression of P2RY(14) in the S1HL.