Class
Article
College
College of Science
Department
Biology Department
Faculty Mentor
Erin Bobeck
Presentation Type
Poster Presentation
Abstract
First-line chemotherapies against solid tumors are highly efficacious in reducing the tumor burden, but have many adverse side-effects including nerve damage, leading to chronic pain. Non-addictive, efficacious pain relievers are an area of active interest, and we propose a novel target to address this pressing issue. GPR171 is a G-Protein Coupled Receptor that was recently deorphanized and was identified to be expressed in the brain in regions that regulate reward, anxiety, and pain. Within the pain circuit, it was shown previously that systemic administration of the GPR171 agonist enhances morphine antinociception in acute pain tests. Preliminary data from our lab has shown that GPR171 activation can also alleviate persistent inflammatory pain. However, the role of this receptor has not been investigated in other chronic pain models. Given these findings in acute and inflammatory pain, we hypothesize that GPR171 can reduce neuropathic pain. To test this hypothesis, we investigate the role of GPR171 in chronic neuropathic pain. We tested the efficacy of a GPR171 agonist in a chemotherapy-induced neuropathy mouse model. Neuropathic pain was induced by injecting paclitaxel (16 mg/kg) followed by assessment of mechanical pain thresholds using Von Frey filaments. Our results indicate that the GPR171 agonist can relieve neuropathic pain. In addition, using immunofluorescence we observed that mice with neuropathic pain show a decrease in GPR171 receptors within a key brain region involved in pain modulation, the periaqueductal gray (PAG). Overall, this study proposes that GPR171 may be a novel target for the treatment of neuropathic pain. Presentation Time: Thursday, 1-2 p.m.
Location
Logan, UT
Start Date
4-9-2021 12:00 AM
Included in
Role of Novel Receptor GPR171 in Chemotherapy-Induced Neuropathic Pain
Logan, UT
First-line chemotherapies against solid tumors are highly efficacious in reducing the tumor burden, but have many adverse side-effects including nerve damage, leading to chronic pain. Non-addictive, efficacious pain relievers are an area of active interest, and we propose a novel target to address this pressing issue. GPR171 is a G-Protein Coupled Receptor that was recently deorphanized and was identified to be expressed in the brain in regions that regulate reward, anxiety, and pain. Within the pain circuit, it was shown previously that systemic administration of the GPR171 agonist enhances morphine antinociception in acute pain tests. Preliminary data from our lab has shown that GPR171 activation can also alleviate persistent inflammatory pain. However, the role of this receptor has not been investigated in other chronic pain models. Given these findings in acute and inflammatory pain, we hypothesize that GPR171 can reduce neuropathic pain. To test this hypothesis, we investigate the role of GPR171 in chronic neuropathic pain. We tested the efficacy of a GPR171 agonist in a chemotherapy-induced neuropathy mouse model. Neuropathic pain was induced by injecting paclitaxel (16 mg/kg) followed by assessment of mechanical pain thresholds using Von Frey filaments. Our results indicate that the GPR171 agonist can relieve neuropathic pain. In addition, using immunofluorescence we observed that mice with neuropathic pain show a decrease in GPR171 receptors within a key brain region involved in pain modulation, the periaqueductal gray (PAG). Overall, this study proposes that GPR171 may be a novel target for the treatment of neuropathic pain. Presentation Time: Thursday, 1-2 p.m.