Previous studies have established a relationship between marijuana use and risky behavior in natural settings. A limited number of laboratory investigations of marijuana effects on human risk taking have been conducted. The present study was designed to examine the acute effects of smoked marijuana on human risk taking, and to identify behavioral mechanisms that may be involved in drug-induced changes in the probability of risky behavior. Using a laboratory measure of risk taking designed to address acute drug effects, 10 adults were administered placebo cigarettes and three doses of active marijuana cigarettes (half placebo and half 1.77%; 1.77%; and 3.58% D 9 -THC) in a within-subject repeated-measures experimental design. The risk-taking task presented subjects with a choice between two response options operationally defined as risky and nonrisky. Data analyses examined cardiovascular and subjective effects, response rates, distribution of choices between the risky and nonrisky option, and first-order transition probabilities of trial-by-trial data. The 3.58% THC dose increased selection of the risky response option, and uniquely shifted response probabilities following both winning and losing outcomes following selection of the risky option. Acute marijuana administration thereby produced measurable changes in risky decision making under laboratory conditions. Consistent with previous risk-taking studies, shifts in trial-by-trial response probabilities at the highest dose suggested a change in sensitivity to both reinforced and losing risky outcomes. Altered sensitivity to consequences may be a mechanism in drug-induced changes in risk taking. Possible neurobiological sites of action related to THC are discussed. Neuropsychopharmacology (2005) 30, 800-809.

Two experiments evaluated rate dependency and a neuropharmacological model of timing as explanations of the effects of amphetamine on behavior under discriminative control by time. Four pigeons pecked keys during 60-trial sessions. On each trial, the houselight was lit for a particular duration (5 to 30 s), and then the key was lit for 30 s. In Experiment 1, the key could be lit either green or blue. If the key was lit green and the sample was 30 s, or if the key was lit blue and the sample was 5 s, pecks produced food on a variable-interval 20-s schedule. The rate of key pecking increased as a function of sample duration when the key was green and decreased as a function of sample duration when the key was blue. Acute d-amphetamine (0.1 to 3.0 mg/kg) decreased higher rates of key pecking and increased lower rates of key pecking as predicted by rate dependency, but did not shift the timing functions leftward (toward overestimation) as predicted by the neuropharmacological model. These results were replicated in Experiment 2, in which the key was lit only one color during sessions, indicating that the effects were not likely due to disruption of discriminative control by key color. These results are thus consistent with rate dependency but not with the predictions of the neuropharmacological model.

It has long been known that acute marijuana administration impairs working memory (e.g., the discrimination of stimuli separated by a delay). The determination of which of the individual components of memory are altered by marijuana is an unresolved problem. Previous human studies did not use test protocols that allowed for the determination of delay-independent (initial discrimination) from delay-dependent (forgetting or retrieval) components of memory. Using methods developed in the experimental analysis of behavior and signal detection theory, we tested the acute effects of smoked marijuana on forgetting functions in 5 humans. Immediately after smoking placebo, a low dose, or a high dose of marijuana (varying in delta9-THC content), subjects completed delayed match-to-sample testing that included a range of retention intervals within each test session (0.5, 4, 12, and 24 s). Performances (discriminability) at each dose were plotted as forgetting functions, as described and developed by White and colleagues (White, 1985; White & Ruske, 2002). For all 5 subjects, both delta9-THC doses impaired delay-dependent discrimination but not delay-independent discrimination. The outcome is consistent with current nonhuman studies examining the role of the cannabinoid system on delayed matching procedures, and the data help illuminate one behavioral mechanism through which marijuana alters memory performance.

Alprazolam administration produced increases in human risk taking under laboratory conditions. In union with previous studies, the observed shift in trial-by-trial response probabilities suggests that sensitivity to consequences (e.g., oversensitivity to recent rewards) may be an important mechanism in the psychopharmacology of risky decision making. Additionally, risk-seeking personality traits may be predictive of acute drug effects on risk-taking behavior.