CaMKII binding to GluN2B at S1303 Has No Role in Acute or Inflammatory Pain.

CaMKII binding to GluN2B at S1303 Has No Role in Acute or Inflammatory Pain.
Brain Res. 2020 Oct 14;:147154
Authors: Maduka UP, White SR, Joiner MA, Hell JW, Hammond DL
Abstract
Activation of Ca2+/calmodulin kinase II (CaMKII) and the N-Methyl D-aspartate receptor (NMDAR), particularly its GluN2B subunit, contribute to the central sensitization of nociceptive pathways and persistent pain. Using mutant mice wherein the activity-driven binding of CaMKII to S1303 in GluN2B is abrogated (GluN2BKI), this study investigated the importance of this interaction for acute and persistent inflammatory nociception. GluN2BKI, wild type and heterozygote mice did not differ in responses to acute noxious heat stimuli as measured with tail flick, paw flick, or hot plate assays, nor did they differ in their responses to mechanical stimulation with von Frey filaments. Surprisingly, the three genotypes exhibited similar spontaneous pain behaviors and hypersensitivity to heat or mechanical stimuli induced by intraplantar injection of capsaicin; however, GluN2BKI mice did not immediately attend to the paw. WT and GluN2BKI mice also did not differ in the nociceptive behaviors elicited by intraplantar injection of formalin, even though MK801 greatly reduced these behaviors in both genotypes concordant with NMDAR dependence. CaMKII binding to GluN2B at S1303 therefore does not appear to be critical for the development of inflammatory nociception. Finally, int...

Source: Brain Research - October 14, 2020 Category: Neurology Authors: Maduka UP, White SR, Joiner MA, Hell JW, Hammond DL Tags: Brain Res Source Type: research