The nucleus accumbens (NAcc) is an integral part of the basal ganglia located within the ventral striatum. It is composed of two regions: core and shell which has been related to reward motivated behavior. It is positioned as an interface between the limbic and motor systems integrating signals arising from these structures, and to modulate limbic drive and motor planning. The NAcc is innervated by limbic structures and receives convergent excitatory afferents from the ventral hippocampus, basolateral amygdala (BLA) and medial prefrontal cortex. In addition, it receives dopaminergic input from the ventral tegmental area (VTA) which has been implicated in a number of functions related to neural reward processing. In the last years our laboratory has characterized the influences of several brain structures modulating synaptic plasticity in the dentate gyrus (DG) of the hippocampal formation. Synaptic plasticity characterized by changes in the efficacy of synaptic transmission at synapses, can contribute to storage of information within neural circuits. Two major forms of long-term changes in synaptic efficacy have been characterized: long-term potentiation (LTP) and long-term depression (LTD). These changes in synaptic strength can occur both on short-term and long-term basis depending on synaptic activity and the modulatory type of synapse. Characterizing the brain structure in question, it was electrically stimulated within a distinct time window prior to or after short-term plasticity induction in the DG. Under distinct circumstances, activation of modulatory brain structures can transform a protein synthesis-independent early long-term potentiation (early-LTP) to a late long-term potentiation (late-LTP) in the DG. Here, we stimulated the NAcc core or shell 15 minutes after induction of early-LTP in the DG via the perforant pathway (PP) stimulation. Summarizing, the stimulation of NAcc core or shell did not significantly modify the amplitude or the duration of DG early-LTP. Stimulation of the NAcc core 15 minutes prior to the induction of DG early-LTP via the PP completely prevented the induction of early-LTP of the field excitatory postsynaptic potential (f-EPSP) while the population spike amplitude (PSA) potentiated less than control and decayed very fast to baseline value. The stimulation of the NAcc shell before induction of DG early-LTP did neither modify significantly the amplitude nor the duration of DG early-LTP. In a set of control experiments, we investigated if stimulation of the NAcc core or shell alone, without tetanus to the PP, would have an effect on baseline values after stimulating the DG. The results for these control experiments indicated that NAcc core stimulation slightly but significantly depressed the PSA up to 8 h but not f-EPSP. In summary, NAcc stimulation after the induction of early-LTP seems to have no effect on the time course and late phases of the potentiation in the DG. However, NAcc stimulation before the induction of LTP had influences on the time course and the late phases of the potentiation.