TY  - JOUR
A1  - Hohmann, Stephan
A1  - Angioni, Carlo
A1  - Tunaru, Sorin
A1  - Lee, Seungkyu
A1  - Woolf, Clifford J.
A1  - Offermanns, Stefan
A1  - Geisslinger, Gerd
A1  - Scholich, Klaus
A1  - Sisignano, Marco
T1  - The G2A receptor (GPR132) contributes to oxaliplatin-induced mechanical pain hypersensitivity
T2  - Scientific Reports
N2  - Chemotherapy-induced peripheral neuropathic pain (CIPN) is a common and severe debilitating side effect of many widely used cytostatics. However, there is no approved pharmacological treatment for CIPN available. Among other substances, oxaliplatin causes CIPN in up to 80% of treated patients. Here, we report the involvement of the G-protein coupled receptor G2A (GPR132) in oxaliplatin-induced neuropathic pain in mice. We found that mice deficient in the G2A-receptor show decreased mechanical hypersensitivity after oxaliplatin treatment. Lipid ligands of G2A were found in increased concentrations in the sciatic nerve and dorsal root ganglia of oxaliplatin treated mice. Calcium imaging and patch-clamp experiments show that G2A activation sensitizes the ligand-gated ion channel TRPV1 in sensory neurons via activation of PKC. Based on these findings, we conclude that targeting G2A may be a promising approach to reduce oxaliplatin-induced TRPV1-sensitization and the hyperexcitability of sensory neurons and thereby to reduce pain in patients treated with this chemotherapeutic agent.
Y1  - 2017
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/82756
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-827561
SN  - 2045-2322
VL  - 7
IS  - Article number: 446
PB  - Macmillan Publishers Limited, part of Springer Nature
CY  - London
ER  -