TY - JOUR
T1 - GPR55 and GPR119 Receptors Contribute to the Processing of Neuropathic Pain in Rats
AU - Zúñiga-Romero, Ángel
AU - Rivera-Plata, Quetzali
AU - Arrieta, Jesús
AU - Flores-Murrieta, Francisco Javier
AU - Rodríguez-Silverio, Juan
AU - Reyes-García, Juan Gerardo
AU - Huerta-Cruz, Juan Carlos
AU - Ramírez-Martínez, Gustavo
AU - Rocha-González, Héctor Isaac
N1 - Publisher Copyright:
© 2022 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2022/1
Y1 - 2022/1
N2 - Orphan G-protein-coupled receptors (GPCR) comprise a large number of receptors which are widely distributed in the nervous system and represent an opportunity to identify new molecular targets in pain medicine. GPR55 and GPR119 are two orphan GPCR receptors whose physiological function is unclear. The aim was to explore the participation of spinal GPR55 and GPR119 in the processing of neuropathic pain in rats. Mechanical allodynia was evaluated using von Frey filaments. Protein localization and modulation were measured by immunohistochemistry and western blotting, respectively. Intrathecal administration of CID16020046 (selective GPR55 antagonist) or AS1269574 (selective GPR119 agonist) produced a dose-dependent antiallodynic effect, whereas O1062 (GPR55 agonist) and G-protein antagonist peptide dose-dependently prevented the antiallodynic effect of CID16020046 and AS1269574, respectively. Both GPR55 and GPR119 receptors were expressed in spinal cord, dorsal root ganglia and sciatic nerve, but only GPR119 was downregulated after 14 days of spinal nerve ligation. Data suggest that GPR55 and GPR119 participate in the processing of neuropathic pain and could be useful targets to manage neuropathic pain disorders.
AB - Orphan G-protein-coupled receptors (GPCR) comprise a large number of receptors which are widely distributed in the nervous system and represent an opportunity to identify new molecular targets in pain medicine. GPR55 and GPR119 are two orphan GPCR receptors whose physiological function is unclear. The aim was to explore the participation of spinal GPR55 and GPR119 in the processing of neuropathic pain in rats. Mechanical allodynia was evaluated using von Frey filaments. Protein localization and modulation were measured by immunohistochemistry and western blotting, respectively. Intrathecal administration of CID16020046 (selective GPR55 antagonist) or AS1269574 (selective GPR119 agonist) produced a dose-dependent antiallodynic effect, whereas O1062 (GPR55 agonist) and G-protein antagonist peptide dose-dependently prevented the antiallodynic effect of CID16020046 and AS1269574, respectively. Both GPR55 and GPR119 receptors were expressed in spinal cord, dorsal root ganglia and sciatic nerve, but only GPR119 was downregulated after 14 days of spinal nerve ligation. Data suggest that GPR55 and GPR119 participate in the processing of neuropathic pain and could be useful targets to manage neuropathic pain disorders.
KW - Allodynia
KW - GPR119
KW - GPR55
KW - Neuropathic pain
KW - Spinal nerve ligation
UR - http://www.scopus.com/inward/record.url?scp=85139489783&partnerID=8YFLogxK
U2 - 10.3390/ph15010067
DO - 10.3390/ph15010067
M3 - Artículo
C2 - 35056124
AN - SCOPUS:85139489783
SN - 1424-8247
VL - 15
JO - Pharmaceuticals
JF - Pharmaceuticals
IS - 1
M1 - 67
ER -