In the current study, correct response latencies and omission rate were only increased by doses of SR141716A and O-2050 that were higher than those required to reduce premature responding. In addition, feeder latencies were not affected by any drug treatment indicating that the effects of both CB1 receptor Fulvestrant inquirer antagonists were probably unrelated to their anorectic properties. Another putative confounding factor might relate to the implementation of a fixed ITI duration in the current study, as rats could have adapted a timing strategy to help them predict the onset of stimulus presentations, a strategy that might simultaneously decrease premature responding. Consequently, given that both psychostimulants and cannabinoids are known to affect timing behavior, the observed drug effects on premature Reversine Aurora Kinase inhibitor responding might have been a reflection of distorted timing abilities rather than altered impulsivity. However, the observation that both psychostimulants and CB receptor agonists result in an underestimation of time and only psychostimulant administration results in increased premature responding in the 5-CSRTT argues against such an explanation. In addition, it was recently found that the CB1 receptor antagonist SLV330 reduced premature responding in a version of the 5-CSRTT that incorporated ITI durations of variable length rendering stimulus presentation unpredictable in time. Similarly, amphetamine has been shown to increase premature responding in a 5-CSRTT with variable ITI durations, although in this particular study premature responses remained unpunished hampering the interpretation of this parameter as a readout for inhibitory control. Moreover, others have reported a reduction in impulsivity following amphetamine administration under similar conditions. Altogether, these findings do not support amajor role for altered time perception in the drug-induced changes in impulsivity observed in the current study. Collectively, although non-specific behavioral effects of the drugs used in this study cannot be ruled out completely, such effects are unlikely to have fully accounted for the effects of these compounds on impulsivity. Considering the apparent important role of CB1 receptor activity in inhibitory control deficits, it was somewhat surprising that the CB receptor agonist D9-THC did not affect premature responding in the 5-CSRTT. Similar results were previously obtained for another synthetic CB receptor agonist, WIN55,212�C2. Collectively, these data suggest that CB1 receptors regulating inhibitory control may already be maximally activated, for instance, due to excessive task-induced release of endogenous cannabinoids, thereby occluding effects of exogenous CB receptor agonists on impulsivity. Alternatively, distinct populations of CB1 receptors in the brain may exert opposite effects on premature responding.