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

Dopaminergic neurotransmission in the nucleus accumbens (NAc) and neural processes in the basolateral (BLA) and central (CeN) amygdala nuclei are implicated in associative reward learning. Given their direct and indirect connections with the NAc and ventral tegmental area (VTA), both the BLA and CeN may regulate the mesoaccumbens dopamine (DA) system in rewarding situations. Electrical stimulation of the BLA (20 Hz, 10 sec, 300 microA) induced a long-lasting 25 +/- 4% increase in DA efflux in the NAc, measured by microdialysis in freely moving rats, whereas comparable stimulation of the CeN had no effect. Reverse dialysis of either the NMDA receptor antagonist APV (100 micrometer) or the AMPA-kainate receptor antagonist DNQX (100 micrometer), but not the metabotropic glutamate receptor antagonist (+/-)-amino-4-carboxy-methyl-phenylacetic acid (100 micrometer), into the NAc blocked the stimulation-evoked increase in DA efflux in the NAc. VTA infusion of lidocaine (lido; 4%) significantly reduced basal DA levels for approximately 30 min but failed to suppress the increase in NAc DA efflux resulting from BLA stimulation. Additionally, infusions of lido (4%) into the medial prefrontal cortex failed to block the stimulation-evoked increase in NAc DA efflux. These data support the hypothesis that the BLA can directly modulate DA efflux through local mechanisms in the NAc, independent of an action on DA cell bodies in the VTA. The finding that brief activation of the CeN had no long-lasting effects on DA efflux in the NAc suggests an important degree of functional independence between the CeN and BLA.