Using 3-T proton magnetic resonance spectroscopy (1H-MRS), Gallinat et al. [199] have suggested the involvement of glutamatergic neurotransmission in integrative frontal-hippocampal processing [199] and the sensation seeking personality dimension [200]. The study demonstrated a strong relationship between glutamate levels in the hippocampus and frontal theta activity during auditory stimulus processing [199]. Glutamatergic neurotransmission and its neuroadaptive changes have been proposed as important molecular determinants of craving and relapse [201,202]. In particular, it is suggested that a hyperglutamatergic state mediates, at least in part, alcohol relapse behavior and maintenance of alcoholism [203]. Several studies have suggested the involvement of glutamate receptors, NMDA and metabotropic, in alcohol relapse [204-206]. Acamprosate, a drug used to prevent relapse in alcoholic patients [207], has been suggested to act through a suppression of a hyperglutamatergic state created by alcohol addiction [208,209]. Although there have been as yet no ERO/ERPs studies done in alcoholics during/after the administration of anti-craving/anti-dependence medications, such as acamprosate, naltrexone, etc., a few resting EEG studies in animals [210-212] and in humans [213-215] found EEG alterations after administration of these drugs. While animal
