Figure 1
From: Neuroprotective effects of naltrexone in a mouse model of post-traumatic seizures

Naltrexone normalized MOR signaling in cortex following TBI. (a,b) Western blot analysis of phospho-MOR (S375) and MOR in the CTX tissue extract at 8 days and 3 months post-TBI. TBI increased both S375 phosphorylation (panel 1A) and MOR expression (1b) in the CTX at acute and chronic time-points compared to sham, and NTX treatment (T + N group) significantly reduced the effect of TBI. (c) MOR immunostaining in the CTX. Green represents MOR, and blue is DAPI (d,e). Quantification of MOR-positive cells (with DAPI) in the CTX at (d) 8 days and (e) 3 months post-TBI, both illustrating reduction of MOR-positive cells with NTX treatment. All groups were compared to each other using one-way ANOVA with Tukey’s post-hoc test; *p < 0.05, **p < 0.01, ****p < 0.0001; n = 6–8 (3–4 sections per animal). All the data is represented as standard error mean (SEM). Scale: all 100 μm. S sham, TBI traumatic brain injury, T + N TBI with naltrexone, NTX naltrexone only, without TBI, neocortex (CTX).