88 LH was set at 5 s, and in subsequent sessions, was individually titrated to meet performance criterion of 80% successful hits and <20% prestimulus responses. Omissions of a go stimulus response within the LH resulted in a 5-s time- out period, during which both the houselight and stimulus light were turned off. From initial shaping to criterion performance in this phase, 26 sessions were required. Shaping: introduction stop signal During the final training phase, a stop signal was introduced in 25% of all trials. Initially, this stop signal (duration, 50 ms; frequency, 4,500 Hz; intensity 80 dB) was contingent with the appearance of the go signal. Responding during the onset of the stop signal or during the LH immediately extin- guished the go stimulus and houselight, turned off the stop signal, and was followed by a 5-s time-out. In contrast, if the animal successfully refrained from responding during a stop trial, a pellet was delivered. Initially, the LH during stop and go trials were equal; however, when performance during stop trials was below 80% successfully inhibited stop trials, the LH during stop trials was lowered over sessions in steps of 100–200 ms until animals improved performance. Subsequently, the LH was then gradually increased in these individuals over sessions until the LH during both go and stop trials were equal. As soon as animals reached the criterion of approximately 90% successfully inhibited stop trials, delays for the onset of the stop signal were introduced. The stop-signal delays (SSD) were presented in a pseudorandom order, and to compensate for differences between rats, SSDs were based on each individual rats’ mean reaction time on go trials in the preceding drug-free training session. SSDs were calculated as follows: mRT minus either 25, 50, 100, 200, or 400 ms. In addition, an equal amount of zero delays were presented during sessions. Drug testing commenced upon stable baseline performance for at least five consecutive sessions, i.e., 80% accuracy during go trials and a significant SSD-dependent decrease in correctly inhibited stop trials. It took 30 sessions before animals reached stable baseline performance after the introduction of the stop signal; therefore, from initial shaping to stable baseline performance in the stop-signal paradigm, in total, 56 sessions were required. Stop-signal paradigm: estimation stop-signal reaction time and correction for omissions during go trials Calculations to estimate the stop-signal reaction times (SSRT) and a correction for omission errors were adapted from Logan (1994) and Solanto et al. (2001). For estimating the SSRT, data of the three SSDs of 200, 100, and 50 ms were used, as the probability of correct Psychopharmacology (2007) 193:85–96 inhibition on these intervals was within the range of 0.2< p <0.8, and thus, most informative for estimating SSRT (Band et al. 2003). For each of the three intervals, the probability of responding was calculated including a correction for nonresponses based on the number of omissions during the go trials, the latter, as omissions cannot be distinguished from successful inhibitions during stop trials. The following formula, adapted from Solanto et al. (2001) was used for these calculations: jpðrespondingÞ ¼ ðx correct inhibitionsÞ=x xyj; where x is the number of stop-signal trials at each delay interval; correct inhibitions are the number of correctly inhibited trials, and y is the probability of omissions during the go trials within the entire session. To calculate SSRTs, reaction times on all go trials were rank ordered. From this list with RTs, the “nth” RT was taken, where “n“ was obtained by multiplying the total number of go trials by the probability of responding for a particular SSD. This RT value approximates the latency between onset of the go stimulus and completion of the stopping process. The SSRT for each interval is then obtained by subtracting the SSD interval from this RT. The average estimated SSRT that is used for the analyses in the present study is calculated by taking the mean of each SSRT at the three SSDs (200, 100, and 50 ms). Drugs SR141716A was generated and kindly donated by Solvay Pharmaceuticals (Weesp, The Netherlands), whereas WIN55,212-2 was purchased from Tocris Biosciences (Bristol, United Kingdom). Both SR141716A and WIN55,212-2 were dissolved as described previously in a mixture of ethanol, Tween80, and sterile saline (ratio 1:1:18; cf. De Vries et al. 2001). In all experiments, SR141716A was injected 30 min before testing, whereas WIN55,212-2 was injected 20 min before testing. In all paradigms, the order of testing the drugs was (1) SR141716A and (2) WIN55,212-2. The drug combination was only performed in the five-choice serial reaction time task and followed the studies with SR141716A and WIN55,212-2. Drugs were freshly prepared each day before testing and intraperitoneally injected in a volume of 1 ml/kg bodyweight according to a Latin square design for both the dose–response studies and the drug combina- tion on Tuesdays and Fridays, with baseline training sessions on the other weekdays. Statistical analyses Data were subjected to repeated measures analysis of variance (ANOVA) with drug dose (all paradigms), delay