Brain stimulation reward is affected by D2 dopamine receptor manipulations in the extended amygdala but not the nucleus accumbens.

This work examines the effects on brain stimulation reward (BSR) of D1 and D2 dopamine receptor manipulations in the sublenticular central extended amygdala (SLEAc) and the nucleus accumbens shell (NAc). Fifty-three male Long Evans rats received medial forebrain bundle stimulation electrodes and bilateral injection guide cannulae aimed at either the SLEAc or the NAc. The rate-frequency paradigm was used to assess drug-induced changes in stimulation reward effectiveness and in response rate following 0.50 microl injections of isotonic saline, 5.0mug of SKF38393 (D1 receptor agonist), 2.0 microg of SCH 23390 (D1 blocker), 10.0 microg of quinpirole (D2 agonist) and 3.0 microg of eticlopride (D2 blocker). The drugs were injected both ipsi- and contralateral to the stimulation site. When injected into the NAc none of the drugs affected either the frequency required to maintain half-maximal responding or maximum response rate. D2 receptor blockade in the SLEAc contralateral to the stimulation site significantly but modestly enhanced both the stimulation's reward effectiveness and response rate while D2 receptor agonism decreased responding. Injections into the SLEAc ipsilateral to the stimulation site were ineffective. These results suggest that dopaminergic neurotransmission in the SLEAc is more important to reward processes than is dopamine in the NAc. We align our findings with past work by considering methodological details and a currently hypothesized role for NAc dopamine in learning behaviors that lead to reward capture.