Fig. 4.

PFC receptor mechanisms underlying the divergent dose–response curves of MPH across working memory and sustained attention. a The working memory-enhancing actions of intra-dmPFC (dorsal anterior cingulate/ dorsal prelimbic) MPH (0.125 μg) are blocked with co-infusion of the α2 antagonist atipamezole (1.25 μg) or the D1 antagonist SCH23390 (0.5 μg), but not the α1 antagonist benoxathian (0.4 μg) at doses that alone do not alter performance as measured by the percent change in performance from baseline. Schematic depicts all infusion sites with MPH (squares). b Similar to working memory, the sustained attention-enhancing actions of intra-dmPFC MPH (0.5 μg) were blocked with co-infusion of the α2 antagonist atipamezole (0.625 μg) or the D1 antagonist SCH23390 (0.5 μg). However, in contrast to working memory, the α1 antagonist, benoxathian (0.4 μg), also blocked intra-dmPFC MPH-induced improvements in sustained attention. Consistent with this latter observation, intra-dmPFC infusion of a dose of the α1 agonist, phenylephrine (0.1 μg), previously shown to impair working memory [32, 36] significantly improved sustained attention, as measured by change in d′ from vehicle (mean ± SEM). The magnitude of improvement is comparable to that seen with intra-dmPFC MPH (0.5 μg). Schematic depicts all infusion sites with MPH depicted (squares). Numbers represent anterior/posterior coordinates of coronal sections. Acg dorsal anterior cingulate, PL prelimbic PFC. *p < 0.05, **p < 0.01 compared to vehicle or baseline