Moreover, extracellular DA in different cortices was found to be modified by drugs acting on noradrenergic transmission but not, or only modestly, by drugs modifying dopaminergic activity [9-11]. Thus, consistent with its ability to inhibit noradrenergic activity, the α2-adrenoceptor agonist clonidine produced a concomitant reduction in extracellular DA and NA both in the mPFC and Occ, whereas the α2-adrenoceptor antagonists idazoxan and RS 79948 produced a concomitant increase in extracellular NA and DA in both cortices [10,11]. Moreover, local infusion into the LC of carbachol, kainic acid or N-methyl aspartic acid increased both NA and DA in the mPFC, in accord with their ability to activate noradrenergic neurons [13].