FIG. 2.

Loss of perilesional KCC2 within the first two weeks after traumatic brain injury (TBI) involves dynamic post-translational processing that precedes total protein decline. (A) Peptide-to-protein KCC2 rollup results reflecting post-translational processing within the first two weeks after TBI. Fold change data reported as mean ± standard error of the mean (SEM), n = 6, log2 transformed and normalized to time-zero control. *Q-value corrected to a 5% false discovery rate (FDR). (B) KCC2 immunoblotting reflecting perilesional total protein decline beginning two days after injury. Inset images show KCC2 densitometric results after background subtraction and adjusting for load and transfer variability using matched β-actin staining. Values reported as mean ± SEM across two independent KCC2 antibodies, n = 6/group, Tukey HSD: *p < 0.05. (C) Representative micrographs from barrel cortex layers 4/5 of KCC2 Immunofluorescence staining morphologically depicting perilesional KCC2 neuronal loss (NeuN-stained soma) over the first two weeks after TBI. (D) Post-translational KCC2 dynamics involves n-terminal acetylation and multimodal phosphorylation, shown here at threonine 34 (T34) and serine 649 (S649) across the first two weeks after injury. Fold change data reported as mean ± SEM, n = 6, log2 transformed and normalized to time-zero control. *Q-value corrected to a 5% FDR. CCI, controlled cortical impact.