GluA1 subunit has been proposed to play a role in the adaptation processes mediating the initial steps that eventually lead to compulsive drug use [12]. GluA1−/− mice show various phenotypes related to substance abuse as they i) fail to show cocaine-induced enhancement in AMPA/NMDA ratio in ventral tegmental area dopamine cells (VTA DA cells) [13], ii) display a specific impairment in stimulus reward learning by showing no conditioned reinforcement and abnormal second-order responding [14] and iii) express deficient morphine- and benzodiazepine-induced adaptation during development of tolerance and in withdrawal phase [15], [16].
