Basolateral amygdala dopamine modulation of medial prefrontal cortical and nucleus accumbens dopamine function

Stress activates dopamine (DA) transmission in the basolateral amygdala (BLA), medial prefrontal cortex (mPFC) and nucleus accumbens (NAc), and DA transmission in these regions mediates different aspects of the behavioural response to stress. Evidence indicates that a functional interdependence exists between the DA projections to these areas. mPFC DA exerts an inhibitory influence on stress-induced NAc DA release. Similarly, BLA DA modulates mPFC and NAc DA function, although it is unknown if this is also the case in response to stress. Thus, we examined whether BLA DA modulates NAc and mPFC DA release in response to stress. We first determined the effects of BLA DA depletion on stress-induced NAc and mPFC DA release. BLA DA depletion potentiated the NAc and attenuated the mPFC DA responses to stress. We then examined the effects of intra-BLA D1 and D2/D3 receptor antagonists on the NAc and mPFC DA responses to stress. BLA D1, but not D2/D3, receptor antagonism potentiated and attenuated stress-induced NAc and mPFC DA release, respectively. Co-administration of D1 antagonist into BLA and DA agonists into mPFC abolished the potentiation of stress-induced NAc DA release, indicating that BLA D1 receptor modulation of the NAc DA stress response occurs indirectly by modulating stress-induced mPFC DA release. We then turned to examining the influence of BLA DA on behavioural measures of information processing which are themselves modulated by NAc and mPFC DA function. The effects of BLA D1 and D2/D3 receptor blockade on prepulse inhibition (PPI) and latent inhibition (LI) were examined. BLA D1 receptor antagonist enhanced and D2/D3 receptor antagonist reduced PPI. Conversely, neither BLA DA receptor antagonist had an effect on LI. Finally, we determined the effects of BLA D1 and D2/D3 receptor antagonists on acoustic startle habituation. Although BLA DA receptor antagonism had no effect on this measure, both D1 and D2/D3 receptor blockade redu