Patch-clamp recordings, performed in young mice (P20–26), revealed that the VTA DA neurons of the GluA1−/− mice failed to show glutamate receptor neuroplasticity in the same manner as those of GluA1+/+ mice after a single morphine administration. This deficient neuroplasticity has been observed in the GluA1−/− mice also after cocaine administration [13]. The elevation of AMPA/NMDA receptor current ratio is considered to represent NMDA receptor-dependent long-term potentiation (LTP) in the VTA [20], [29]. Activation of VTA DA neurons by the drugs of abuse elevates the level of GluA1 subunit in the VTA [30], [31]. According to the current hypothesis, the activation of VTA DA neurons leads to a fast insertion of calcium-permeable non-GluA2 subunits (GluA1, GluA3 or GluA4) to their afferent synapses, which provide an additional source of calcium, leading to LTP [32]–[34]. Impaired LTP may be more general in 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
