Psychopharmacology (2007) 193:85–96 91 Fig. 2 Coadministration of WIN55,212-2 at 1.0 mg/kg (WIN1) prevents the effects of 3.0 mg/kg SR14716A (SR3) on inhibitory control in the 5-CSRTT. All data are depicted as mean (±SEM). *p< 0.05 and **p<0.005 at any of the tested doses [dose: F3,45 = 1.28, p = 0.29 and dose × SSD: F12,180 = 1.25, p = 0.26]; however, the percent- age of correctly inhibited stop trials significantly declined with decreasing stop-signal delays [SSD: F4,60 = 39.24, p < 0.001]. SR141716A did slow mean reaction times during go trials by approximately 30 ms [Fig. 4b; dose: F3,45 = 7.93, p = 0.001], and further analyses indicated that both the 1.0 and 3.0 mg/kg dose significantly slowed reaction times compared with vehicle. Nonetheless, the number of omissions during go trials were not significantly affected [mean ± SEM: vehicle = 16.2 ± 3.0; 0.3 mg/kg = 18.1 ± 1.2; 1.0 mg/kg = 17.7 ± 1.7 and 3.0 mg/kg = 23.3 ± 2.6; dose: F3,45 = 1.76, p = 0.17]. Lastly, the average estimated SSRT across three stop-signal delays, putatively reflecting re- sponse inhibition, was not significantly changed by SR141716A at any dose [Fig. 4c; dose: F3,45 = 1.47, p = 0.24]. Furthermore, a median split analysis (median SSRT: 238 ms) did not reveal differential effects of SR141716A on the estimated SSRT in individuals with relatively “fast” vs “slow” stopping abilities [slow vs fast stopper: F1,14 = 9.54, p = 0.008; dose: F3,42 = 1.04, p = 0.38 and dose × slow vs fast stopper: F3,42 = 2.48, p = 0.074]. In the WIN55,212-2 experiments, at the highest dose, in total, four animals did not start any go trials and were therefore excluded from all stop-signal data analyses. Response inhibition, as displayed in the inhibition function curve in Fig. 5a, was affected by WIN55,212-2 [SSD: F4,44= 23.51, p< 0.001; dose: F3,33= 5.12, p= 0.005 and dose× SSD: F12,132= 1.11, p= 0.36], and further comparisons revealed that 0.3 mg/kg WIN55,212-2 significantly deteriorated the Fig. 3 Effects of SR141716A (a) and WIN55,212-2 (b) on the mean (±SEM) percentage preference for the large reinforcer in the delayed reward paradigm percentage of correct inhibition compared to vehicle. Mean reaction times during go trials were slowed by WIN55,212-2 [Fig. 5b; dose: F3,33= 15.07, p< 0.001], and further analyses indicated that 1.0 and 3.0 mg/kg WIN55,212-2 significantly slowed mean reaction times compared to vehicle. Nonethe- less, the number of omissions during go trials were not significantly affected [mean ± SEM: vehicle = 14.8 ± 1.9; 0.3 mg/kg=23.2±4.8; 1.0 mg/kg=26.1±5.4 and 3.0 mg/kg= 34.7±7.0; dose: F3,33=3.06, p=0.073]. Lastly, the average estimated SSRT across three stop-signal delays, putatively reflecting response inhibition, was not significantly changed by WIN55,212-2 at any dose [Fig. 5c; dose: F3,33=2.06, p= 0.13]. Furthermore, a median split analysis (median SSRT: 227 ms) did not reveal differential effects of WIN55,212-2 on the estimated SSRT in individuals with relatively “fast” vs “slow” stopping abilities [slow vs fast stopper: F1,10=9.57, p= 0.011; dose: F3,30=2.12, p=0.12 and dose×slow vs fast stopper: F3,30=1.30, p=0.29].