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The goal of the present experiment was to examine the effect of certain (deceptive) strategies (e.g., false denial) on memory. Specifically, participants were shown a traumatic virtual reality (VR) video of an airplane crash. Following this, participants (N= 94) received questions concerning details from the VR scene in a baseline memory task. Then, participants could choose from 3 options how to cope in response to having experienced the VR scene: tell the truth, falsely deny, or fabricate. The majority opted to tell the truth (n = 81). A subsample of truth tellers were instructed to falsely deny having seen certain details. One week later, all participants received a source monitoring task in which they were asked (1) whether they remembered talking about these details during an interview, and (2) whether they remembered seeing certain details during the VR experience the week before. Participants had to tell the truth during this task. Participants who were instructed to falsely deny showed impaired memory for presented details that had previously been discussed (i.e., denial-induced forgetting) and seen in the VR scene. Also, the presentation of certain details in the baseline memory task seemed to inoculate participants who were instructed to falsely deny from experiencing memory impairment. The current experiment suggests that false denials can have adverse ramifications for memory for what is discussed and seen. ispartof: MEMORY & COGNITION vol:47 issue:3 pages:485-495 ispartof: location:United States status: published

The human eye-movement system is equipped with a sophisticated updating mechanism that can adjust for large retinal displacements produced by saccadic eye movements. The nature of this updating mechanism is still highly debated. Previous studies have demonstrated that updating can occur very rapidly and is initiated before the start of a saccade. In the present study, we used saccade curvature to demonstrate that the oculomotor system is tuned for detecting object displacements during saccades. Participants made a sequence of saccades while ignoring an irrelevant distractor. Curvature of the second saccade relative to the distractor was used to estimate the time course of updating. Saccade curvature away from the presaccadic location of the distractor emerged as early as 80 ms after the first saccade when the distractor was displaced during a saccade. This is about 50 ms earlier than when a distractor was only present before a saccade, only present after a saccade, or remained stationary across a saccade. This shows that the oculomotor system prioritizes detection of object displacements during saccades, which may be useful for guiding corrective saccades. The results also challenge previous views by demonstrating the additional role of postsaccadic information in updating target-distractor competition across saccades.

Acute stress is known to affect the way we process rewards. For example, during, or directly after stress, activity within key brain areas of the reward circuitry is reduced when a reward is presented. Generally, the effects of stress on the brain are time-dependent, changing neural and cognitive processing in the aftermath of stress to aid recovery. Such a dynamic response to stress is important for resilience on the longer term. However, relatively little is known about reward processing during the recovery phase of stress and whether this is changed in individuals at increased risk for stress-related psychopathology.Healthy male individuals (N = 40) and unaffected siblings of schizophrenia patients (N = 40) were randomized to either an acute stress task (Trier Social Stress Test) or a no-stress task. Neural responses during reward anticipation and reward feedback (monetary gain or no gain) were examined 50 min later using an fMRI monetary incentive delay task. The ventral striatum and orbitofrontal cortex (OFC) were used as predefined hypothesis-driven regions of interest.Neural responses following stress differed between controls and siblings during reward feedback (group-stress interaction OFC p = 0.003, ventral striatum p = 0.031), showing increased ventral striatum and OFC responses following stress in healthy controls only. Exploratory analyses revealed that this effect was most pronounced during hit trials (compared to when a reward was omitted), and independent of monetary value. Stress did not affect subsequent reward processing in siblings of schizophrenia patients. We found no significant differences between controls and siblings in ventral striatum and OFC responses during reward anticipation following stress.This study shows that ventral striatum and OFC responses to positive task feedback are increased in the aftermath of stress in healthy male controls, regardless of monetary value. This indicates a dynamic shift from previously reported reduced responses in the striatum and OFC to reward feedback directly after stress to increased responses to both reward and non-reward feedback during the recovery phase of stress. These increased neural responses following stress were absent in siblings of schizophrenia patients. Together, these findings indicate that stress recovery is affected in this at-risk group, particularly in responses to positive feedback following stress.

Dysfunctional patterns of activation in brain reward networks have been suggested as a core element in the pathophysiology of schizophrenia. However, it remains unclear whether this dysfunction is specific to schizophrenia or can be continuously observed across persons with different levels of nonclinical and clinical symptom expression. Therefore, we sought to investigate whether the pattern of reward system dysfunction is consistent with a dimensional or categorical model of psychosis-like symptom expression. 23 patients with schizophrenia and 37 healthy control participants with varying levels of psychosis-like symptoms, separated into 3 groups of low, medium, and high symptom expression underwent event-related functional magnetic resonance imaging while performing a Cued Reinforcement Reaction Time task. We observed lower activation in the ventral striatum during the expectation of high vs no reward to be associated with higher symptom expression across all participants. No significant difference between patients with schizophrenia and healthy participants with high symptom expression was found. However, connectivity between the ventral striatum and the medial orbitofrontal cortex was specifically reduced in patients with schizophrenia. Dysfunctional local activation of the ventral striatum depends less on diagnostic category than on the degree of symptom expression, therefore showing a pattern consistent with a psychosis continuum. In contrast, aberrant connectivity in the reward system is specific to patients with schizophrenia, thereby supporting a categorical view. Thus, the results of the present study provide evidence for both continuous and discontinuous neural substrates of symptom expression across patients with schizophrenia and the general population.

Many theories of human sexual behavior assume that sexual stimuli obtain arousing properties through associative learning processes. It is widely accepted that classical conditioning contributes to the etiology of both normal and maladaptive human behaviors. Despite the hypothesized importance of basic learning processes in sexual behavior, research on classical conditioning of the sexual response in humans is scarce. In the present paper, animal studies and studies in humans on the role of pavlovian conditioning on sexual responses are reviewed. Animal research shows robust, direct effects of conditioning processes on partner- and place preference. On the contrast, the empirical research with humans in this area is limited and earlier studies within this field are plagued by methodological confounds. Although recent experimental demonstrations of human sexual conditioning are neither numerous nor robust, sexual arousal showed to be conditionable in both men and women. The present paper serves to highlight the major empirical findings and to renew the insight in how stimuli can acquire sexually arousing value. Hereby also related neurobiological processes in reward learning are discussed. Finally, the connections between animal and human research on the conditionability of sexual responses are discussed, and suggestions for future directions in human research are given.

INTRODUCTION: Extinction involves an inhibitory form of new learning that is highly dependent on the context for expression. This is supported by phenomena such as renewal and spontaneous recovery, which may help explain the persistence of appetitive behavior, and related problems such as addictions. Research on these phenomena in the sexual domain is lacking, where it may help to explain the persistence of learned sexual responses.METHOD: Men (n = 40) and women (n = 62) participated in a differential conditioning paradigm, with genital vibrotactile stimulation as US and neutral pictures as conditional stimuli (CSs). Dependent variables were genital and subjective sexual arousal, affect, US expectancy, and approach and avoid tendencies towards the CSs. Extinction and renewal of conditioned sexual responses were studied by context manipulation (AAA vs. ABA condition).RESULTS: No renewal effect of genital conditioned responding could be detected, but an obvious recovery of US expectancy following a context change after extinction (ABA) was demonstrated. Additionally, women demonstrated recovery of subjective affect and subjective sexual arousal. Participants in the ABA demonstrated more approach biases towards stimuli.CONCLUSIONS: The findings support the context dependency of extinction and renewal of conditioned sexual responses in humans. This knowledge may have implications for the treatment of disturbances in sexual appetitive responses such as hypo- and hypersexuality.