Fig. 6
From: Chronically altered NMDAR signaling in epilepsy mediates comorbid depression
Comparison of physiological and pathological NMDAR signaling as suggested by the findings in this study. Long-term pathological changes following excitotoxic injury result in the predominance of the NR2B subunit of NMDAR which inhibits downstream ERK signaling upon overstimulation. Furthermore, these long-term changes lead to the constitutive activity of nNOS and increased NO levels, resulting in mitochondrial impairment, inhibition of protein synthesis, and direct inhibition of ERK signaling through nitrosylation