• A Ishikawa, F Ambroggi, S M Nicola, and H L Fields.
• Ernest Gallo Clinic & Research Center, University of California, San Francisco, 5858 Horton Street, Suite 200, Emeryville, CA 94608, USA. akinori@yamaguchi-u.ac.jp
• Neuroscience. 2008 Aug 26; 155 (3): 573584573-84.

AbstractReward-seeking behavior is controlled by neuronal circuits that include the basolateral nucleus of amygdala (BLA), medial prefrontal cortex (mPFC), nucleus accumbens (NAc) and ventral tegmental area. Using a discriminative stimulus (DS) task in which an intermittently presented cue (DS) directs rats to make an operant response for sucrose, we previously demonstrated that dopamine receptor antagonism in the NAc reduced reinforced cue responding, whereas general inactivation of the NAc increased behavioral responding in the absence of the cue. Because they send major glutamatergic projections to the NAc, the BLA and mPFC may also contribute to reward-seeking behaviors modulated by the NAc. In this study we compare the effects of BLA and mPFC inactivation on rats' performance of a DS task. BLA inactivation by combined GABA(A) and GABA(B) agonists impaired cue responding with minimal effects on operant behavior in the absence of cues. Dorsal medial prefrontal cortex (dmPFC) inactivation also inhibited cue-evoked reward-seeking. In contrast, ventral medial prefrontal cortex (vmPFC) inactivation disinhibited responding to unrewarded cues with less influence on reinforced cue responding. These findings demonstrate that the BLA and dmPFC facilitate cue-evoked reward-seeking, whereas, in the same task the vmPFC exerts inhibitory control over unrewarded behaviors.

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