Dopamine release within the nucleus accumbens (NAcc) has been associated with both the rewarding and locomotor-stimulant effects of abused drugs. The functions of the NAcc core and shell were investigated in mediating amphetamine-potentiated conditioned reinforcement and locomotion. Rats were initially trained to associate a neutral stimulus (Pavlovian CS) with food reinforcement (US). After excitotoxic lesions that selectively destroyed either the NAcc core or shell, animals underwent additional CS-US training sessions and then were tested for the acquisition of a new instrumental response that produced the CS acting as a conditioned reinforcer (CR). Animals were infused intra-NAcc with D-amphetamine (0, 1, 3, 10, or 20 microg) before each session. Shell lesions affected neither Pavlovian nor instrumental conditioning but completely abolished the potentiative effect of intra-NAcc amphetamine on responding with CR. Core-lesioned animals were impaired during the Pavlovian retraining sessions but showed no deficit in the acquisition of responding with CR. However, the selectivity in stimulant-induced potentiation of the CR lever was reduced, as intra-NAcc amphetamine infusions dose-dependently increased responding on both the CR lever and a nonreinforced (control) lever. Shell lesions produced hypoactivity and attenuated amphetamine-induced activity. In contrast, core lesions resulted in hyperactivity and enhanced the locomotor-stimulating effect of amphetamine. These results indicate a functional dissociation of subregions of the NAcc; the shell is a critical site for stimulant effects underlying the enhancement of responding with CR and locomotion after intra-NAcc injections of amphetamine, whereas the core is implicated in mechanisms underlying the expression of CS-US associations.

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The effects of bilateral excitotoxic lesions of 3 major sources of afferents to the ventral striatum (nucleus accumbens) were compared on an open field test of food neophobia allowing the choice between familiar and novel food. Whereas lesions of the basolatera] amygdala and ventral subiculum had qualitatively similar effects to reduce food neophobia (although not affecting the latency to eat), amygdala lesions increased and the ventral subiculum decreased locomotor activity. In contrast, damage to the ventromedial prelimbic prefrontal cortex only affected initial food choice and latency' measures. By comparison, excitotoxic lesions of the nucleus accumbens itself and intra-accumbens infusion of the TV-methyl-D-aspartate (NMDA) receptor antagonist APS increased activity and attenuated food neophobia. Results are discussed in terms of the role of limbic and prefrontal neuronal networks converging in the nucleus accumbens to control different aspects of the behavioral response to novelty.It is now apparent that the functioning of the ventral striatum, including the nucleus accumbens (n. accumbens), is determined by its so-called limbic afferents from the amygdala, hippocampal formation, and prelimbic corlex. Mogcnson (1984) investigated functional interactions between the limbic system and the striatum using a combined electrophysiological and behavioral approach that focused on the control of locomotor activity by output of the n. accumbens, controlled in turn by its limbic input and modulated by the ascending mesolimbic dopamine system. This approach arose from two distinct lines of work: one demonstrating a special role for the n. accumbens in the control of spontaneous and drug-induced locomotor activity, and the other characterizing the role of the limbic system in mediating behavioral and aversive responses to novelty, including aversion and exploration. Thus, dopaminedependent mechanisms of the n. accumbens mediate the locomotor stimulant effect of amphetamine in the rat