Glutamate receptor-dependent modulation of dopamine efflux in the nucleus accumbens by the basolateral, but not the central, nucleus of the amygdala in rats

Dopaminergic neurotransmission in the nucleus accumbens (NAc) has been implicated in reward-related behavior. Recent experiments have described distinct roles of the central (CeN) and basolateral (BLA) amygdala nuclei in the context of associative rewardrelated learning. Given their direct and indirect connections to the NAc and ventral tegmental area (VTA), both the BLA and CeN may interact with the mesoaccumbens DA system during associative learning. The present experiments were designed to test if electrical stimulation of the BLA or CeN could increase dopamine (DA) efflux in the NAc. Microdialysis combined with HPLC-ED was used to monitor NAc DA efflux in freely moving rats. Results revealed that stimulation of the BLA (20 Hz, 10 sec, 300 μA) induced a long-lasting 25±4% increase in NAc DA efflux whereas CeN stimulation had no effect. Reverse dialysis of either the NMDA receptor antagonist AP-V (100 μM) or the AMPA/kainate receptor antagonist DNQX (100 μM), but not the metabotropic glutamate receptor antagonist MCPG (100 μM), into the NAc blocked the stimulationinduced increase in DA efflux in the NAc. Intra-VTA infusion (2 uL, 0.5 μL/min, unilateral) of the reversible sodium channel blocker lidocaine (4%) significantly reduced basal DA levels for ~ 30 minutes but failed to suppress the increase in NAc DA efflux resulting from BLA stimulation. Consequently, we suggest that afferents from the BLA directly modulate DA efflux at the terminals in the NAc, not the cell bodies in the VTA. Results are discussed in the context of limbic-striatal interactions and associative learning.Arts, Faculty ofPsychology, Department ofGraduat