Figure 5.

The ability of vigabatrin treatment to decrease the association of the receptor α1 subunit with calnexin is not due to the activation of surface GABA_A or GABA_B receptors. High-density neuronal cultures were treated for 3 h at 37°C with (A) DMSO (control) or the GAT blocker NCC 05-2090 (100 μM), (B) vehicle (control) or the GABA_B receptor agonist baclofen (100 μM), or (C) vehicle (control), VGB (0.5 μg/μl), VGB (0.5 μg/μl) + the GABA_A receptor channel blocker PTX (100 μM) or PTX (100 μM). Neuronal lysates were immunoprecipitated with an anti-α1 subunit antibody and SDS PAGE/Western blotting was performed with anti-α1 subunit and anti-calnexin antibodies. Representative blots are shown in (A–C). (D) Replicate data (n ≥ 3) of experiments in (A–C). Neuronal cultures from different litters were used for experiments in (A–C). Data for each experiment were normalized to their respective controls and assembled into one graph. Immunoreactive bands were quantified densitometrically and data are presented as the average ± SEM. A one-way ANOVA performed on the data set from experiments in C yielded a p value of 0.0013. Post hoc significance differences (Tukey’s multiple comparison) between C vs. VGB and C vs. VGB + PTX were observed (*p ≤ 0.05). No statistically significant difference was observed between VGB vs. VGB + PTX treatment groups.