BASOLATERAL AMYGDALA STIMULATION EVOKES GLUTAMATE RECEPTOR-DEPENDENT DOPAMINE EFFLUX IN THE NUCLEUS-ACCUMBENS OF THE ANESTHETIZED RAT

Afferents from the basolateral amygdala and dopamine projections from the ventral tegmental area to the nucleus accumbens have both been imp licated in reward-related processes. The present study used in vivo ch ronoamperometry with stearate-graphite paste electrodes in urethane-an aesthetized rats to determine how basolateral amygdala efferents to th e nucleus accumbens synaptically regulate dopamine efflux. Repetitive- pulse (20 Hz for 10 s) electrical stimulation of the basolateral amygd ala evoked a complex pattern of changes in monitored dopamine oxidatio n currents in the nucleus accumbens related to dopamine efflux. These changes were characterized by an initial increase that was time-locked to stimulation, a secondary decrease below baseline, followed by a pr olonged increase in the dopamine signal above baseline. The effects of burst-patterned stimulation (100 Hz, 5 pulses/burst, 1-s interburst i nterval, 40 s) of the basolateral amygdala on the basal accumbens dopa mine signal were similar to those evoked by 20 Hz stimulation, with th e lack of a secondary suppressive component. Infusions of the ionotrop ic glutamate receptor antagonists (+/-)-2-amino-5-phosphonopentanoic a cid (APV) or 6,7-dinitroquinoxaline-2,3-dione (DNQX) into the nucleus accumbens dose-dependently blocked or attenuated the initial and prolo nged increases in the dopamine signal following 20 Hz or burst-pattern ed basolateral amygdala stimulation. Infusions of the metabotropic glu tamate receptor antagonist (+)-alpha-methyl-4-carboxyphenylglycine sel ectively blocked the intermediate suppressive effect of 20 Hz basolate ral amygdala stimulation on dopamine oxidation currents. Blockade of g lutamate receptors or inhibition of dopamine neuronal activity via inf usions of either APV + DNQX, lidocaine or gamma-hydroxybutyric acid, r espectively, into the ventral tegmental area did not effect the patter n of changes in the accumbens dopamine signal evoked by basolateral am ygdala stimulation. These data suggest that the glutamatergic basolate ral amygdala inputs to nucleus accumbens dopamine terminals synaptical ly facilitate or depress dopamine efflux, and these effects are indepe ndent of dopamine neuronal firing activity. Moreover, these results im ply that changes in nucleus accumbens dopamine levels following presen tation of reward-related stimuli may be mediated, in part, by the baso lateral amygdala.