90 cantly increased the percentageof accurate choice from ap- proximately 77% under vehicle conditions to 82% as shown in Table 1 [F3,45=3.43, p=0.025]. In addition, a marginal, but significant, increase in the latency to make a correct choice was also detected, and further comparisons showed that only the high dose of 3.0 mg/kg significantly slowed correct re- sponse reaction time [Table 1; F3,45=4.53, p=0.007]. The la- tency to collect a food reward and errors of omission, however, were not affected at any dose [Table 1; feeder latency: F3,45= 0.39, p=0.65 and omissions: F3,45=1.30, p=0.29]. WIN55,212-2 did neither change the number of prema- ture responses nor the number of perseverative responses after correct choice [Fig. 1c and d; premature responses: F3,45 = 1.02, p =0.39 and perseverative responses: F3,45= 1.64, p =0.21; respectively]. Furthermore, as indicated in Table 1, WIN55,212-2 did not change accurate choice or the latency to collect a pellet after correct choice [accurate choice: F3,45 =0.72, p= 0.54 and feeder latency: F3,45= 3.19, p =0.052]. In contrast, errors of omission were increased, and latencies to make a correct choice were lengthened by WIN55,212-2 [omissions: F3,45 = 7.44, p= 0.002 and correct response latency: F3,45 = 6.59, p= 0.004]. As shown in Fig. 2, the decrements in premature responding by 3.0 mg/kg SR141716A were prevented in the presence of WIN55,212-2 at a dose of 1.0 mg/kg [F3,45= 7.33, p < 0.001]. In addition, this selected dose of WIN55,212-2, by itself, did not affect inhibitory control as indicated by the absence of an effect of this dose on the number of premature responses. SR141716A and WIN55,212-2 do not affect decision making in the delayed reward paradigm Stable baseline performance on the delayed reward paradigm occurred after approximately 30 training sessions on a full delay range (0, 10, 20, 40, and 60 s), and therefore, we commenced drug testing from session 35 onwards. A clear, highly significant delay-dependent decrement in the percent- age preference for the large reinforcer was observed [Fig. 3; Psychopharmacology (2007) 193:85–96 delay: F4,60=270.22, p<0.001]. Nonetheless, SR141716A did not shift the preference for a large reinforcer over delays at any of the tested doses [dose: F3,45=1.56, p=0.21 and dose × delay: F12,180 = 1.24, p = 0.29]. In addition, SR141716A also did not change the total numbers of omitted choice trials, i.e., the failures to start a trial during the choice phase [dose: F3,45=3.10, p=0.052]. In the WIN55,212-2 experiments, at the highest dose, in total, five animals omitted all choice trials of some delays, and therefore, were excluded from all analyses of the delay discounting data. Similar to SR141716A, increasing the delay highly significantly shifted the preference from large to the small reinforcer [Fig. 4; delay: F4,40 =179.06, p< 0.001]. Although there was no overall effect of WIN55,212-2 on decision making [dose: F3,30 =0.68, p= 0.57], there was a dose by delay interaction effect suggesting a shift in preference for the large reinforcer over delays [dose × delay: F12,120 =2.61, p= 0.011]. None- theless, further post hoc comparisons revealed no differ- ences between vehicle and any of the other doses. The number of omitted choice trials was not affected by WIN55,212-2 [dose: F3,30 = 1.61, p =0.21]. Effects of SR141716A and WIN55,212-2 on response inhibition in the stop-signal paradigm Under baseline conditions in the stop-signal paradigm, there was stable individual variation in mean reaction times during go trials over consecutive sessions ranging from 290 to 470 ms (mean: 365 ms; standard deviation: 58 ms). Likewise, the limited hold periods during go and stop trials also stably varied and ranged from 400 to 1,100 ms (mean: 594 ms; SD: 167 ms). A highly significant positive correlation indicated that individuals with “shorter” limited hold periods also displayed shorter mean go reaction times compared to individuals with “longer” limited hold periods that were slower in go reaction speed [r= 0.85, p < 0.001]. Response inhibition, as displayed in the inhibition function curve in Fig. 4a, was not affected by SR141716A Table 1 Effects of SR141716A and WIN55,212-2 on measures of attentional function and motivation in the 5-CSRTT. Data depict mean± SEM *p<0.05 **p<0.005 vs vehicle Accuracy (%) Response latency (ms) Omissions (%) Feeder latency (ms) SR141716A Vehicle 0.3 mg/kg 1.0 mg/kg 3.0 mg/kg WIN55,212-2 Vehicle 0.3 mg/kg 1.0 mg/kg 3.0 mg/kg 77.2±2.4 82.0±1.9* 80.5±2.5 80.2±2.3 77.7±2.5 79.6±2.3 77.2±2.3 76.8±2.7 336±9 338±10 347±14 374±14* 324±7 333±10 380±23* 399±17** 5.4±1.1 5.6±1.0 5.1±0.7 7.3±1.0 3.9±0.7 3.4±0.7 14.4±4.3* 20.2±4.1** 954±48 954±44 937±43 939±37 956±53 910±41 943±44 1212±138