Studies have shown that gp120-induced release of mediators from Schwann cells induce CCR5-dependent DRG neurotoxicity, however, CCR5 antagonists failed to improve pain in HIV- infected individuals.
The OVX mice showed reduced pain sensitivity compared to sham, suggesting a role of the ovarian hormones in sex differences in pain sensitivity to gp120.
We report here that HIV-1 gp120, a neurotoxic protein that is specifically associated with the manifestation of pain in HIV patients, induces synapse loss via microglia.
<b>Methods:</b> The paw withdrawal threshold and the paw withdrawal latency were observed to assess pain behaviors in all groups of the rats, including control group, control combined with Andro treatment group, sham group, gp120 combined with ddC treatment group, gp120 plus ddC combined with A438079 treatment group, and gp120 plus ddC combined with Andro treatment by intrathecally injecting at a dose of 25 μg/20 μl group.
Young adult male rats (Sprague-Dawley) were stereotaxically pretreated with HIV-1 envelope glycoprotein 120 (gp120) into the periaqueductal gray (PAG) area, the primary control center of pain modulation.
In this study, we aimed to explore the role of the P2X<sub>7</sub> receptor in gp120-induced neuropathic pain using a rat model specific for this type of pain.