Fig. 3From: Blocking glycine receptors reduces neuroinflammation and restores neurotransmission in cerebellum through ADAM17-TNFR1-NF-κβ pathwayBlocking glycine receptor normalizes membrane expression of the TNFα receptor TNFR1 through a PKC and ADAM17-dependent mechanism. Membrane expression of TNFR1 (a and c) and ADAM17 (b and d) were analyzed using BS3 cross-linker procedure as described in the “Methods” section in slices from control and hyperammonemic (HA) rats treated with strychnine (inhibitor of glycine receptor) or bisindolyl (PKC inhibitor). The phosphorylation at Tyr204 of ErK (e), at Thr180/Tyr182 of p38 (f), and at Thr735 of ADAM17 (g) were analyzed by western blot in slices from control and hyperammonemic rats treated or not with strychnine. Phosphorylation levels were normalized to the total amount of the respective proteins (Erk, p38 and ADAM17) and to the control for protein loading (GADPH or actin). Values are the mean ± SEM of 12–41 rats per group. Values significantly different from control rats are indicated by asterisk and from hyperammonemic rats are indicated by “a”. *p < 0.05, **p < 0.01, ****p < 0.0001; a p < 0.05, aa p < 0.01, aaaa p < 0.0001. Data were analyzed using a one-way analysis of variance (ANOVA) followed by Turkey post hoc (in a, c, e, and f) and the non-parametric Kruskal-Wallis test followed by Dunnett’s post hoc test (in b, d, and g)Back to article page