320 Fig. 3 Effects of amphetamine (a), the selective DA reuptake inhibitor GBR12909 (b), the selective reuptake inhibitor atomoxetine (c) and the selective 5-HT reuptake inhibitor citalopram (d) on the percentage choice for the large reinforcer in the delayed reward paradigm. In total, n=13–15 animals were included in the analysis. Asterisk indicates p<0.05 and two asterisks indicates p<0.01 compared to vehicle treatment (paired samples t-test). All data are expressed as mean±SEM Psychopharmacology (2012) 219:313–326 did not affect impulsive choice. Furthermore, using a long ITI in the 5-CSRTT, we show that amphetamine and the DA reuptake blocker GBR12909 enhance, and that atom- oxetine and citalopram reduce impulsive action. Thus, the effects of these drugs on impulsive behavior were not qualitatively different under baseline and long ITI con- ditions. Consistent with previous findings, we also show that amphetamine and the selective dopamine reuptake blocker GBR12909 decreased impulsive choice. Amphetamine has been consistently reported to disrupt inhibitory control, i.e., the ability to withhold responding in the 5-CSRTT (Cole and Robbins 1987; 1989; Harrison et al. 1997; Murphy et al. 2008; Paterson et al. 2011; Pattij et al. 2007; Sun et al. 2011; Van Gaalen et al. 2006a). Our findings confirmed this disinhibitory effect of amphet- amine, which increased the number of premature responses in the 5-CSRTT at all doses tested (0.25–1 mg/kg). In addition to response inhibition, the 5-CSRTT provides several relatively independent measures of performance such as task efficiency, motivation and attentional capacity (Robbins 2002). Alongside its effects on premature responding, amphetamine also attenuated accuracy, en- hanced perseverative responding, reduced response latency (at 0.5 mg/kg only) and had biphasic effects on errors of omission. The effects of amphetamine were comparable under baseline and long ITI conditions. Although not universally reported as effects of amphetamine in the 5- CSRTT, the present profile of effects is highly comparable to previous reports (reduced accuracy: Cole and Robbins 1989; Harrison et al. 1997; Pattij et al. 2007; Sun et al. 2011; increased omissions: Cole and Robbins 1987; 1989; Harrison et al. 1997; Murphy et al. 2008; Sun et al. 2011; Van Gaalen et al. 2006a; and faster response latency: Cole and Robbins 1987; 1989; Harrison et al. 1997; Pattij et al. 2007). Amphetamine increases extracellular levels of DA, NA, and, to a lesser extent, 5-HT by binding to monoamine transporters on the cell membrane and on intracellular neurotransmitter storage vesicles as a false substrate thereby promoting reverse transport of cytosolic transmitter stores (Seiden et al. 1993; Sulzer et al. 1995). Comparable to amphetamine, GBR12909 also enhanced premature responding, reduced accuracy, enhanced perseverative responding and reduced response latencies under both baseline and long ITI conditions. This indicates that the effects of amphetamine in the 5-CSRTT—except for the increases in errors of omission at the highest dose—are mediated by DA (Fernando et al. 2011; Seu et al. 2009; Van Gaalen et al. 2006a). Pharmacological studies have shown that the amphetamine-induced augmentation of premature responding in the 5-CSRTT largely depends on DA D2 receptor stimulation in the nucleus accumbens (Cole and Robbins 1989; Pattij et al. 2007; Van Gaalen et al. 2006a; 2009). Conversely, reducing DA neurotransmission using DA receptor antagonists or low doses of DA D2 receptor agonists, which suppress DA neurotransmission by stimu-