Figure 5.

Pharmacological analysis of DA/NA interaction. A, NA application (50 μm, 1 min) induced a membrane depolarization that was unaffected by pretreatment with 10 μmSCH23390 (a). Similarly, the excitatory effect caused by 100 μm DA was not prevented by betaxolol (10 μm) (b). Conversely, bath-applied DA (100 μm, 1 min) was able to depolarize the cell via D1 DA receptor activation. In fact, SCH23390 (10 μm) prevented the DA response (c). In the presence of SCH23390, high DA concentrations (300 μm) were still able to induce a residual membrane depolarization. The addition of betaxolol (10 μm) to the perfusing solution blocked the DA-induced depolarizing response (d). The membrane depolarization induced by NA (50 μm) occluded the excitatory response to DA. Indeed, at the steady-state level of the NA response, the cell was repolarized by injecting negative current into the cell (150 pA); in this condition DA application was ineffective (e). B, Bath application of cocaine (30 μm) caused a slow membrane depolarization, fully blocked by pretreatment with the D1-like DA receptor antagonist SCH23390 (10 μm) (a). Instead, the selective NA uptake blocker desipramine (100 μm) caused no change in the resting membrane potential of the recorded interneuron (b).