Research reportThe P2X7 receptor in dorsal root ganglia is involved in HIV gp120-associated neuropathic pain

- Upregulation of DRG P2X7 in HIV-associated neuropathic pain.
- Upregulated P2X7 was accompanied with elevated IL-1β and TNF-α expression.
- BBG decreased IL-1β and TNF-α expression and increased IL-10 expression.
- BBG decreased gp120-induced mechanical hyperalgesia via decreasing P2X7.

Human immunodeficiency virus (HIV)-associated neuropathic pain is common, and studies have shown that HIV envelope glycoprotein 120 (gp120) can directly stimulate primary sensory afferent neurons causing hyperalgesia. The P2X7 receptor in the dorsal root ganglia (DRG) is involved in pain transmission and is closely related to the inflammatory and immune response. In this study, we aimed to explore the role of the P2X7 receptor in gp120-induced neuropathic pain using a rat model specific for this type of pain. The results showed that mechanical hyperalgesia, thermal hyperalgesia and P2X7 expression levels were increased in rats treated with gp120. The P2X7 antagonist, brilliant blue G (BBG), decreased hyperalgesia and P2X7 expression levels in rats treated with gp120. BBG also decreased IL-1β and TNF-α receptor expression and ERK1/2 phosphorylation levels and increased IL-10 expression in the gp120-treated rat DRG. In addition, P2X7 agonist (BzATP)-activated currents in DRG neurons cultured with gp120 were larger than those in control neurons, and the inhibitory effect of BBG on BzATP-induced currents in gp120-treated DRG neurons was larger than that in control neurons. Therefore, inhibition of the P2X7 receptor in rat DRG relieved gp120-induced mechanical hyperalgesia and thermal hyperalgesia.