94 comparable dose ranges between 0.3 and 3.0 mg/kg (Lichtman 2000; Takahashi et al. 2005; Terranova et al. 1996; Wolff and Leander 2003). Although the mechanisms responsible for the beneficial effects of disrupting endo- cannabinoid signaling on mnemonic and attentional pro- cesses need to be elucidated further, it is interesting to note that SR141716A increases, among others, cholinergic neurotransmission in the medial prefrontal cortex in vivo (Tzavara et al. 2003). This finding may be particularly relevant for attentional function, as performance in the 5- CSRTT has been shown to be accompanied by increments in acetylcholine release in the medial prefrontal cortex (Passetti et al. 2000), whereas decrements in acetylcholine release in this brain region have been shown to correlate with poor visuospatial attention (McGaughy et al. 2002). A different measure of impulsivity we studied was impulsive choice in the delayed reward paradigm. Concep- tually, impulsive choice differs from inhibitory control in the 5-CSRTT and rather reflects a cognitive decision- making process, as rats have to weigh the immediate vs delayed outcomes of their behavior. Impulsive choice then is reflected in insensitivity towards the delayed larger reward and a preference for the small immediate reward. In the present experiments, we observed that neither SR141716A nor WIN55,212-2 did have any effects on impulsive choice. In accordance with these findings, it has been shown recently that THC did not change delay and probability discounting in human volunteers (McDonald et al. 2003), and together, these data suggest that the (endo) cannabinoid system is not critically involved in impulsive choice. Our observations do contrast with previous findings indicating that marijuana elevates risk-taking behavior in volunteers (Lane et al. 2005). Risk taking, however, differs from delay and probability aversion in that it is most likely to occur when the behavioral options may result in losses or have aversive consequences (Rachlin et al. 1986). In the delayed reward paradigm and the paradigm used by McDonald et al. (2003), subjects could only win and not lose reward (food or money, respectively), whereas only the magnitude of the reward depended upon choice. It is therefore possible, that these procedural and conceptual differences explain the discrepancy in findings, and further- more, that delay aversion and risk-taking processes are differentially regulated by the (endo)cannabinoid system. While response inhibition has been shown to be impaired in human volunteers after THC administration (McDonald et al. 2003), neither disruption of endocanna- binoid signaling nor administration of a CB1 receptor agonist had clear observable behavioral effects on stop- signal task performance. In agreement with the assumption of a “race model” between “go” and “stop” processes (Logan 1994) and previous stop-signal data in rats (Eagle and Robbins 2003a, b), the probability of successfully Psychopharmacology (2007) 193:85–96 inhibiting a response during a stop trial decreased in rats when the onset of the stop signal was delayed in time. Although SR141716A did not shift this inhibition curve as a function of increasing stop-signal delays, the low dose WIN55,212-2 (0.3 mg/kg) significantly deteriorated the ability to inhibit responding with increasing stop-signal delays. However, the primary parameter in this paradigm, the average estimated stop-signal reaction time, or simply put, speed of stopping, was not changed by any dose of SR141716A or WIN55,212-2. In addition, median split analyses revealed no differential drug effects in individuals with “slow” vs “fast” stopping abilities as has been reported previously for the effects of D-amphetamine on stopping speed in both rats and humans (De Wit et al. 2002; Feola et al. 2000). Collectively, our findings suggest that response inhibition processes, as measured in the stop-signal para- digm, are not under control of CB1 receptors. In the present study, the speed of stopping was estimated from separate SSRTs obtained from three stop-signal delays (200, 100, and 50 ms before mean go RT), and consistent with this estimation method, there was some variability in the SSRTs depending on the delay (Band et al. 2003; Logan 1994), with shorter stop-signal delays resulting in SSRTs of approximately 140 ms and longer delays resulting in SSRTs of approximately 300 ms. However, the variability in SSRTs over delays was similar across all doses of both drugs (data not shown), thus, ruling out the possibility that this variability may have masked effects of SR141716A or WIN55,212-2 on response inhibition. In contrast to the measures of response inhibition, reaction times during performance on go trials were slowed by both compounds in line with their effects in the 5-CSRTT. With regard to these effects of SR141716A, in the absence of changes on omission errors in both the 5-CSRTT and the stop signal paradigm, they cannot be solely interpreted in terms of motor effects. Rather, the minor but significant increase in response latencies of approximately 30 ms in both paradigms (Table 1 and Fig. 4b) may indicate changes in information processing speed induced by blockade of endocannabinoid signaling. However, this notion is not confirmed by previous sensorimotor gating data (Mansbach et al. 1996; Martin et al. 2003). In contrast, the effects of 1.0 and 3.0 mg/kg WIN55,212-2 on reaction times in the stop-signal paradigm may in part be secondary to changes in locomotor activity, as these doses also increased the number of omissions in the 5-CSRTT. Remarkably, although both the stop-signal paradigm and 5-CSRTT measure aspects of impulsive action, only inhibitory control in the 5-CSRTT was improved by SR141716A. Impulsive action in the latter paradigm is mainly measured as the inability to inhibit inappropriate (premature) responses, whereas in the stop-signal paradigm impulsive action is reflected in the inability to inhibit