Prefrontal cortex and basolateral amygdala modulation of dopamine-mediated locomotion in the nucleus accumbens core.

The prefrontal cortex (PFC) and the basolateral amygdala (BLA) play a critical role in the production of normal and abnormal goal-oriented behaviors. Though this may be of critical importance to better understand the neural mechanisms of motivated behaviors and certain psychiatric diseases, the specific role of the glutamatergic afferents arising from the PFC and the BLA in the modulation of locomotion produced by activation in the nucleus accumbens (NAcc) of D1-like receptors or D2-like postsynaptic receptors yet has not been examined. Here, we investigated how focal administration of lidocaine in the PFC or the BLA modulated hyperlocomotion induced by injection in the NAcc core of (i) the selective D1-like receptor agonist, SKF 38393, (ii) co-injection of SKF 38393 and of the selective D2-like receptor agonist LY 171555, a pharmacological condition required for the full expression of the postsynaptic effects of D2-like receptor agonists and believed to produce a locomotor response mainly mediated by D2-like postsynaptic receptors (iii) amphetamine, a psychoactive drug that possesses catecholamine and other neurotransmitters releasing effects. We show that reversible inhibition by lidocaine of the PFC potentiated hyperlocomotion induced by d-amphetamine or activation of D2-like postsynaptic receptors. Contrasting with these effects, inhibition by lidocaine of the BLA inhibited hyperlocomotion induced by D1-like receptor activation and amphetamine, but not by D2-like receptor activation. These data demonstrate that the glutamatergic inputs arising from the PFC and the BLA specifically control D2-like- and D1-like-mediated locomotor responses, respectively.