As was expected due to the ability of GHB to block the firing of DA neurons, microdialysis sampling revealed that acute GHB administration in awake rats leads to a decrease in striatal DA compared with baseline levels [12, 13]. In turn, the pharmacokinetic/pharmacodynamic model allowed detection of an IC50 increase in the GHB inhibition of the DA synthesis rate following chronic exposure to GHB, indicating decreased DA sensitivity toward the GHB inhibitory action [13].
