Increased amphetamine-induced locomotion during inactivation of the basolateral amygdala

At low doses, amphetamine has been shown to produce reliable increases in locomotor activity through its actions on the mesolimbic dopamine (DA) terminals in the nucleus accumbens (NAC). The basolateral amygdala (BLA) has recently been reported to have anatomical projections to the NAC, suggesting that it might serve to alter or modulate the function of the NAC. To test this hypothesis, the current experiment produced lidocaine-reversible lesions of the BLA and assessed changes in NAC function by examining alterations in locomotor activity in response to s.c. amphetamine (2mg/kg). While BLA inactivation alone was found to have no effect on spontaneous or basal locomotor activity, it produced a significant potentiation of amphetamine-induced hyperactivity. These results suggest that BLA inactivation removes a system that inhibits the locomotor response to amphetamine. The data are, therefore, consistent with the view that the BLA may serve to modulate NAC function.