the GluA1−/− mice, as LTP is also absent in the hippocampal CA1 area of these mice [10]. The baseline AMPA/NMDA ratio of the GluA1−/− mice was elevated, in agreement with Dong et al. [13]. The mechanism of this alteration is not known and interestingly, genome-wide expression profiling has revealed no upregulation of GluA3 (or ectopic GluA4) expression, but apparently compensatory upregulation of calcium channels in the GluA1−/− mice [35]. It should be noted that, in addition to changes in excitatory inputs to VTA DA neurons, the global knockout of GluA1 subunit in GluA1−/− mice might have induced some unknown changes during nervous system development. Nevertheless, the maximal elevation in the AMPA/NMDA ratio was unlikely reached in GluA1−/− mice since the morphine-induced AMPA/NMDA ratio was higher in GluA1+/+ mice than in GluA1−/− mice.
