Fig. 4.
The cystine–glutamate antiporter is regulated by group II mGluR autoreceptors via a PKA-dependent mechanism. The uptake of [35S]cystine in striatal tissue slices was measured in the presence and absence of the group II agonist APDC, the group II antagonist APICA, the PKA activator Sp-cAMPS, or the PKA inhibitor Rp-cAMPS (n = 4–10/group). Data are presented as [35S]cystine uptake in the presence of inhibitors expressed as percentage of change of [35S]cystine uptake in the absence of inhibitors. A one-way ANOVA on [35S]cystine uptake indicated a significant effect of drug concentration for APDC alone (F(3,27) = 5.34; p< 0.05), APDC plus APICA (F(3,9) = 5.23; p < 0.05), and Rp-cAMPS (F(1,3) = 10.47; p< 0.05). *p < 0.05, difference from [35S]cystine uptake in the absence of inhibitors (Fisher's LSD post hoc analysis).