498 individuals with a low baseline SSRT and better stopping abilities, morphine seemed to “impair” response inhibition by increasing the SSRT. In contrast, in “slow” stopping rats with higher baseline SSRTs, morphine seemed to “improve” response inhibition by decreasing the SSRT. These findings suggest baseline-dependent effects of morphine on response inhibition that could not be detected when the data were calculated over the entire population of rats. This conclusion should be drawn with caution, as we only explored such a relationship by correlation analyses and did not preselect groups of individuals based on response inhibition capacities. Notwithstanding this limitation, various clinical and preclinical studies have indeed supported this notion and shown that the behav- ioral effects of, e.g., amphetamine, in healthy volunteers (De Wit et al. 2000, 2002) as well as amphetamine and methylphenidate in rats on response inhibition largely seem to depend on baseline performance (Feola et al. 2000; Eagle et al. 2007). The observation that morphine shifted more self- controlled decisions by decreasing preference for the large over small reward in our delayed reward paradigm is in line with previous observations in rats (Kieres et al. 2004) and numerous findings of delay discounting in opiate users (Clark et al. 2006; Madden et al. 1997; Petry et al. 1998; Kirby and Petry 2004). With regard to these observations in human opiate users, it is unclear whether increased delay discounting in opiate users results from premorbid levels of impulsive decision making or is the consequence of chronic opiate abuse. Our findings and those of Kieres et al. (2004) at least suggest acute effects of opiates on impulsive decision making. While opiate addicts generally discount the value of delayed monetary rewards or the drug itself, in the present study, rats were food-restricted and highly palatable food pellets served as food reinforcement. Given the involvement of the central opioid system in food reward, and in particular its modulatory role on the hedonic properties of appetitive foods (e.g., Solinas and Goldberg 2005; for review, see Cota et al. 2006), it is possible that morphine might have enhanced the hedonic property of the highly palatable food pellets to the extent that rats shifted their preference from larger delayed food reward to immediate reward. Nonetheless, the finding that the number of omissions to initiate a trial, a parameter that reflects aspects of food- motivated behavior in the delayed reward paradigm (Cardinal et al. 2000), did neither decrease following morphine nor increase following naloxone argues against such an explanation. Similarly, in the 5-CSRTT experi- ments, neither morphine nor naloxone altered the primary indices of food-motivated behavior, namely, the feeder latency and number of omissions at doses that increased impulsivity (Table 1). Psychopharmacology (2009) 205:489–502 It is important to emphasize that the highest morphine dose modestly reduced the preference for the large reward at the 0-s delay by approximately 15% compared to vehicle. This observation may confound a solid interpretation of morphine’s effects on impulsive choice. It is not entirely clear what caused these effects, and this observation is not unique to the present study. In previous experiments, pharmacological challenges with, e.g., ethanol, the 5- HT1A and 5-HT2 receptor agonists 8-OH-DPAT and DOI, and the dopamine D1 receptor antagonist SCH23390 have also been found to reduce the preference for the large reward at the 0-s delay (Evenden and Ryan 1999; Van Gaalen et al. 2006b; Winstanley et al. 2005). As discussed above, effects on food-motivated behavior seem an unlikely explanation, although positive reinforcing drugs including morphine are known to possess aversive stimulus properties and elicit conditioned taste aversions (Hunt and Amit 1987). The observation that following 6.0 mg/kg morphine rats still earned and consumed a similar amount of pellets compared to baseline training and vehicle conditions (data not shown) argues against morphine-induced emetic effects. Alternatively, it is possible that morphine caused difficulties for the animals to distinguish between two behavioral outcomes or induced a positional bias. However, if the former is the case, the question remains why—on average —this only applied to two out of ten choice trials at the 0-s delay and did not result in chance performance throughout the entire session. The finding that similar doses of morphine did not induce a positional bias in the 5-CSRTT (data not shown) does not support such an explanation. Also, if morphine did bias the responses of the animals towards one side of the operant chamber, one would expect animals to always choose either the immediate small reward or delayed large reward irrespective of the delay. Although few individuals (n = 2 in the morphine dose–response experiment and n= 1 in the morphine–naloxone experiment) did indeed display biased responding with 6.0 mg/kg morphine, excluding these individuals from the analyses did not change the overall effects of morphine on delay discounting. Importantly, all other animals highly preferred the large reward at short delays and shifted their preference with longer delays, although in the large majority of animals, the preference for the large reward at the 0-s delay was modestly reduced when treated with 6.0 mg/kg morphine. Analyses on the steepness of the delay discount- ing curves suggest that the effects of morphine became stronger after repeated exposure. Whereas in the dose– response study with morphine the slope of the delay discounting curve with vehicle did not differ from 6.0 mg/kg, in the morphine–naloxone study, the steepness of these curves did differ significantly. Although specu- lative, perhaps tolerance to putative behavioral “disrup- tive” effects of morphine at the 0-s delay explains these