Posttranslational Nitration of Tyrosine Residues Modulates Glutamate Transmission and Contributes to N-Methyl-D-aspartate-Mediated Thermal Hyperalgesia
Figure 3
Inhibition of NMDA-induced hyperalgesia by FeTM-4-PyP5+ is associated with inhibition of spinal protein nitration ((a)–(c)). As shown by immunoprecipitation, the time at which the NMDA mediated hyperalgesia was at its peak (40 minutes), nitration of GluN2B was observed at the level of the spinal cord ((a), (b)). FeTM-4-PyP5+ (2 nmol given 15 min before NMDA) attenuates spinal GluN2B nitration ((a), (b)). Immunoprecipitation data shown in (a) are representative of at least 6 gels from 3 different animals performed on different days. Bar graph in (b) represents quantification by densitometric analysis. No difference for GluN2B or β-actin expression was detected among the lanes in these conditions. † compared to vehicle and * compared to NMDA alone.
