Redox-dependent activation of protein kinase G1α contributes to transient receptor potential cation channel subfamily V member 1-mediated acute nociceptive pain behavior.

ABSTRACT: Sensory neurons relay the pain signals to the brain via the nociceptive system. Notably, reactive oxygen species (ROS) serve as signaling molecules in the somatosensory system; however, their contribution to sensing noxious stimuli remains poorly understood. Herein, the role of protein kinase G (PKG)1α, which is highly expressed in sensory neurons and serves as a ROS target, was investigated in sensory neurons in the processing of acute nociceptive pain. Cys42Ser PKG1α-knock-in (PKG1α-KI) mice, devoid of redox-dependent PKG1α activation, were subjected to behavioral testing, ROS detection assays, gene expression experiments, and imaging analyses. Interestingly, PKG1α-KI mice showed reduced behavioral responses to noxious heat and the transient receptor potential cation channel subfamily V

SUBMITTER: Berg T 

PROVIDER: S-EPMC12379704 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature