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This study showed that accuracy of the estimated relationship between a fictitious symptom and a disease depends on the interaction between the frequency of judgment and the last trial type. This effect appeared both in positive and zero contingencies (Experiment 1), and judgments were less accurate as frequency increased (Experiment 2). The effect can be explained neither by interference of previous judgments or memory demands (Experiment 3), nor by the perceptual characteristics of the stimuli (Experiments 4 and S), and instructions intended to alter processing strategies do not produce any reliable effect. The interaction between frequency and trial type on covariation judgment is not predicted by any model (either statistical or associative) currently used to explain performance in covariation detection. The authors propose a belief-revision model to explain this effect as an important response mode variable on covariation learning.Animals and humans behave adaptively because they are able to detect the relationship between events (Alloy & Tabachnik, 1984;Killeen, 1981;Mackintosh, 1977). Knowledge on covariation or correlation is very important to the organisms' cognitive functioning (Kareev, 1995) because it is needed in order to carry out such tasks as classical conditioning, category learning, or causal induction (Kareev, 1995;Waldmann & Holyoak, 1992). Therefore, it is important to understand the conditions and the mechanisms underlying this ability. A lot of data exists on these topics in the animal conditioning literature, and some authors have argued that human contingency judgments are useful for these purposes (Shanks, 1987). In fact, recent reviews (Allan, 1993;Shanks, 1993;Young, 1995) have stressed the similarity between human contingency judgments and the animal conditioning data. These studies usually use two dichotomous variables; a cue (S) and an outcome (O), with present or absent conditions possible for each. These conditions produce four types of trials: (a) the signal and the outcome are presented together; (b) S but not O occurs; (c) only O is present; and (d) neither S nor O is shown.Human contingency judgments are affected by conditions such as contiguity (Reed, 1992;Shanks, Pearson, & Dickinson, 1989), outcome value (Chatlosh, Neunaber, & Wasserman, 1985), cue competition (blocking [Chapman & Rob-

Impulsivity is tightly linked to addiction. However, there are several pathways by means of which impulsive individuals are more prone to become addicts, or to suffer an addiction more intensely and for a longer period. One of those pathways involves an inadequate appraisal or regulation of positive and negative emotions, leading to lack of control over hazardous behaviors, and inappropriate decisions. In the present work, we assessed cocaine-dependent individuals (CDI; n = 20), pathological gamblers (PG; n = 21), and healthy controls (HC; n = 23) in trait impulsivity measures (UPPS-P model's dimensions), and decision-making tasks (Go/No-go; delay-discounting task). During the Go/No-go task, electroencephalographic (EEG) activity was recorded, and Go/No-go stimuli-evoked potentials (ERP) were extracted. Theory-driven ERP analyses focused on the No-go > Go difference in the N2 ERP. Our results show that negative urgency is one of the several psychological features that distinguish addicts from HC. Nevertheless, among the dimensions of trait impulsivity, negative urgency is unique at independently covarying with gambling over-pathologization in the PG sample. Cocaine-dependent individuals performed more poorly than gamblers in the Go/No-go task, and showed abnormal Go/No-go stimuli-evoked potentials. The difference between the No-go stimulus-evoked N2, and the Go one was attenuated by severity and intensity of chronic cocaine use. Emotional dimensions of impulsivity, however, did not influence Go/No-go performance.

BackgroundThe Stimulus Preceding Negativity (SPN) is a non-motor slow cortical potential elicited by temporally predictable stimuli, customarily interpreted as a physiological index of expectancy. Its origin would be the brain activity responsible for generating the anticipatory mental representation of an expected upcoming event. The SPN manifests itself as a slow cortical potential with negative slope, growing in amplitude as the stimulus approximates. The uncertainty hypothesis we present here postulates that the SPN is linked to control-related areas in the prefrontal cortex that become more active before the occurrence of an upcoming outcome perceived as uncertain.Methods/FindingsWe tested the uncertainty hypothesis by using a repeated measures design in a Human Contingency Learning task with two levels of uncertainty. In the high uncertainty condition, the outcome is unpredictable. In the mid uncertainty condition, the outcome can be learnt to be predicted in 75% of the trials. Our experiment shows that the Stimulus Preceding Negativity is larger for probabilistically unpredictable (uncertain) outcomes than for probabilistically predictable ones. sLoreta estimations of the brain activity preceding the outcome suggest that prefrontal and parietal areas can be involved in its generation. Prefrontal sites activation (Anterior Cingulate and Dorsolateral Prefrontal Cortex) seems to be related to the degree of uncertainty. Activation in posterior parietal areas, however, does not correlates with uncertainty.Conclusions/SignificanceWe suggest that the Stimulus Preceding Negativity reflects the attempt to predict the outcome, when posterior brain areas fail to generate a stable expectancy. Uncertainty is thus conceptualized, not just as the absence of learned expectancy, but as a state with psychological and physiological entity.

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