Amphetamine effects in Nucleus Accumbens core (cNAc)
A different situation was observed in the cNAc. In fact, neither expression of protein regulating release, nor expression of protein regulating reuptake of glutamate were significantly changed at baseline in SERT-/- rats compared to their wild-type counterpart. In addition, no significant changes in these proteins were observed in the cNAc of SERT+/+ rats exposed to either regimen of AMPH. Conversely, both ShA and LgA may have promoted a significant higher release of glutamate that was accompanied by a higher uptake in the LgA-, but not ShA, exposed in SERT-/-rats. The up-regulation of GLT-1 may represent an adaptive mechanism to buffer the increased release of glutamate, which is absent in ShA-exposed rats. This may indicate that changes in GLT-1 expression reflect compensation in the core, and synergism in the shell (see above). Interestingly, in the cNAc of SERT+/+ rats, we noted that both ShA and LgA to AMPH reduced the expression of GluN2 and GluA2 receptor subunits, an effect observed also for their respective scaffolding proteins, i.e. SAP102, SAP97 and GRIP. Conversely, in SERT-/- rats, LgA, but not ShA, significantly up-regulated the three GluN and the two GluA subunits (with the exception of GluA2 in ShA-exposed rats), an effect that was not accompanied, though, by a parallel enhancement of the expression of their respective scaffolding proteins, pointing towards an AMPH-induced reduction in the stability of glutamatergic synapse of the cNAc of SERT-/- rats.