Post hoc two-sample t tests further showed that this effect was driven by glutamatergic system components, with significant infection-related reduction of EAAT2, GluA2, and Shank3 (all t > 3.00; all p < 0.013; unequal variances assumed, see Fig. 2b), while the amount of GABAAR α1-subunits was not significantly different between infected and uninfected animals (p > 0.13; see Additional file 8). This evidence concerns the gene SLC1A2 and infection.