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.