Quantitative autoradiography and imaging techniques have allowed the detection of high-affinity GHB receptor sites, particularly dense in the neuronal cells of forebrain region such as the striatum - including the nucleus accumbens, hippocampus, and thalamus [9]. A cloning technique allowed identification of a GHB specific receptor that has been postulated to exist in the sites matching the regions of GABAB. [10]. The interaction with GABAB receptors leads to an inhibition in dopamine (DA) release and alters of the EEG profiles, as well as behavioral effects such as sedation, and decreases motor activity [11].