Recovery-from-extinction effects (e.g., spontaneous recovery, renewal, reinstatement, and facilitated reacquisition) have become the focus of much research in recent years. However, despite a great deal of empirical data, there are few theoretical explanations for these effects. This paucity poses a severe limitation on our understanding of these behavioral effects, impedes advances in uncovering neural mechanisms of response recovery, and reduces our potential to prevent relapse after exposure therapy. Towards correcting this oversight, this review takes prominent models of associative learning that have been used in the past and continue to be used today to explain Pavlovian conditioning and extinction, and assesses how each model can be applied to account for recovery-from-extinction effects. The models include the Rescorla-Wagner (1972) model, Mackintosh's (1975) attentional model, Pearce and Hall's (1980) attentional model, Wagner's (1981) SOP model, Pearce's (1987) configural model, McLaren and Mackintosh's (2002) elemental model, and Stout and Miller's (2007) SOCR (comparator hypothesis) model. Each model is assessed for how well it explains or does not explain the various recovery-from-extinction phenomena. We offer some suggestions for how the models might be modified to account for these effects in those instances in which they initially fail.

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r Three conditioned suppression experiments with rats as subjects investigated the influence of higher order associations in determining the response potential of a target stimulus. In these experiments, a Pavlovian conditioned inhibitor was compounded with the target cue during extinction treatment. In Experiment 1, strong d suppression was observed to the target cue that was given extinction treatment in the presence of a conditioned inhibitor, relative to a target that was extinguished with an associatively neutral cue or was extinguished alone, suggestive of enhanced protection from extinction provided by a conditioned inhibitor. This effect was replicated in a sensory preconditioning preparation in Experiment 2; in Experiment 3, in a sensory preconditioning p preparation, this protection effect was retroactively attenuated when the conditioned excitor used to train the t conditioned inhibitor was extinguished following extinction of the target. This provides evidence that, at least in a sensory preconditioning preparation, stimuli that are only indirectly associated with the target cue can contribute to the response potential of that target.

Purpose This article highlights the influence of attention and pain anticipation on pain attenuation. Pain-related trait anxiety was found to moderate the effect that attention strategies impose on pain perception. This article may contribute to clinical treatments quality, where pain attenuation effect is desired. Participants and methods One hundred seven participants, comprising of 72 (67%) females and 35 (33%) males between the age of 17 and 48 (M=22.6, SD =4.36), were used in the analysis. The current study measured the effect of pain anticipation and attention on three aspects of pain perception: threshold, tolerance, and perceived pain intensity. Pain anticipation was manipulated by varying the amount of information given to participants about a future pain stimulus. Attention was manipulated through a sensory focusing task and a distraction task. Participants were randomized into 1) InfoControl group with distraction task trial (n=30), 2) InfoControl group with attention to pain trial (n=26), 3) InfoExtra group with distraction task trial (n=26), or 4) InfoExtra group with attention to pain trial (n=25). The pain stimulus was delivered in a form of heat. The moderating effects of pain-related trait anxiety on these variables were also investigated using Pain Anxiety Symptom Scale Short Form. Results Two structural equation models revealed that anticipation is not a predictor of pain perception and neither did it interact with pain-related trait anxiety. However, attention strategies do significantly relate to pain perception. Furthermore, pain-related anxiety was a significant moderator of attention and pain attenuation. These findings imply that the effectiveness of attention strategies in attenuating pain is affected by individuals’ pain-related trait anxiety. Conclusion The results suggest the importance of appointing the appropriate attention strategy to different individuals with varying level of trait anxiety. Future explorations are necessary to develop a more specific understanding on the nature of information and distractions on pain perception.

Are humans unique in their ability to interpret exogenous events as causes? We addressed this question by observing the behavior of rats for indications of causal learning. Within an operant motor-sensory preconditioning paradigm, associative surgical techniques revealed that rats attempted to control an outcome (i.e., a potential effect) by manipulating a potential exogenous cause (i.e., an intervention). Rats were able to generate an innocuous auditory stimulus. This stimulus was then paired with an aversive stimulus. The animals subsequently avoided potential generation of the predictive cue, but not if the aversive stimulus was subsequently devalued or the predictive cue was extinguished (Exp. 1). In Experiment 2, we demonstrated that the aversive stimulus we used was in fact aversive, that it was subject to devaluation, that the cue-aversive stimulus pairings did make the cue a conditioned stimulus, and that the cue was subject to extinction. In Experiments 3 and 4, we established that the decrease in leverpressing observed in Experiment 1 was goal-directed instrumental behavior rather than purely a product of Pavlovian conditioning. To the extent that interventions suggest causal reasoning, it appears that causal reasoning can be based on associations between contiguous exogenous events. Thus, contiguity appears capable of establishing causal relationships between exogenous events. Our results challenge the widely held view that causal learning is uniquely human, and suggest that causal learning is explicable in an associative framework.Keywords Causal learning . Operant behavior . Causal intervention . Manipulability theory . Associative learning . Sensory preconditioningThe world is malleable and, to survive and reproduce, organisms must learn how and under what conditions their actions will control exogenous events. Causal learning facilitates successful interactions with the environment, such as throwing a switch to illuminate a dark room or pressing a lever to receive food. Actions are commonly viewed as causes of contingent consequences (i.e., outcomes). Provided that there is concordance between the contingent outcome and the subject's motivational state, the probability of the action is widely viewed as reflecting the extent to which the action is perceived as a cause of the outcome. But the basis for concluding that there is a causal relationship between two exogenous events is less clear. In situations in which two events are merely correlated, performing an action to produce one event when the other event is desired would be wasted energy. Thus, distinguishing a cause-effect relationship from mere correlation is critical. The scientific identification of two events as cause and effect is formalized using well-designed experiments; however, individuals outside the laboratory quickly infer causal relationships without such rigor. Even researchers, at some level, must suspect a causal relationship based on mere correlation in order to decide whether it is worth testing a particular manipul...