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Generalization of conditioned fear is adaptive in some situations but maladaptive when fear excessively generalizes to innocuous stimuli with incidental resemblance to a genuine threat cue. Recently, empirical interest in fear generalization as a transdiagnostic explanatory mechanism underlying anxiety-related disorders has accelerated. As there are now several studies of fear generalization across multiple types of anxiety-related disorders, the authors conducted a meta-analysis of studies reporting behavioral measures (subjective ratings and psychophysiological indices) of fear generalization in anxiety-related disorder vs. comparison groups. We conducted systematic searches of electronic databases (conducted from January-October 2020) for fear generalization studies involving anxiety-related disorder groups or subclinical analog groups. A total of 300 records were full-text screened and two unpublished datasets were obtained, yielding 16 studies reporting behavioral fear generalization measures. Random-effects meta-analytic models and meta-regressions were applied to the identified data. Fear generalization was significantly heightened in anxiety-related disorder participants (N = 439) relative to comparison participants (N = 428). We did not identify any significant clinical, sample, or methodological moderators. Heightened fear generalization is quantitatively supported as distinguishing anxiety-related disorder groups from comparison groups. Evidence suggests this effect is transdiagnostic, relatively robust to experimental or sample parameters, and that generalization paradigms are a well-supported framework for neurobehavioral investigations of learning and emotion in anxiety-related disorders. We discuss these findings in the context of prior fear conditioning meta-analyses, past neuroimaging investigations of fear generalization in anxiety-related disorders, and future directions and challenges for the field. ispartof: NEUROPSYCHOPHARMACOLOGY vol:47 issue:9 pages:1652-1661 ispartof: location:England status: published

Acute stress has been found to impair the flexible updating of stimulus-outcome associations. However, there is a lack of studies investigating the effect of acute stress on the flexible updating of stimulus-response associations, like active avoidance responses. The current study used an avoidance reversal learning paradigm to address this question. Sixty-one participants learned that a red dot was associated with an aversive sound, whereas a green dot was not (Pavlovian Acquisition phase). Next, they were trained to avoid the aversive stimulus by selectively pressing a button in response to the red, but not the green, dot (Avoidance Acquisition phase). Subsequently, participants either underwent a stress induction task or a no-stress control task. The flexible updating of expectancies of the US and avoidance responses were assessed after reversal of the original contingencies (Reversal Test). Acute stress did not impair the flexible updating of avoidance responses during the Reversal Test. In contrast, results showed that in the stress group the expectancies of the aversive sound were more in accordance with the reversed contingencies compared to the ratings of control participants. Additionally, cortisol responders avoided less often in comparison to cortisol non-responders. Increased noradrenergic activity in stressed participants was related to impairments in the flexible updating of avoidance responses after contingency reversal, while this association was absent in the control participants. In conclusion, our results suggest that the autonomic response might account for shifting the balance towards inflexible updating of stimulus-outcome awareness while stress does not impair flexible updating of avoidance responses.

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.

Many theories of perception are anchored in the central notion that the brain continuously updates an internal model of the world to infer the probable causes of sensory events. In this framework, the brain needs not only to predict the causes of sensory input, but also when they are most likely to happen. In this article, we review the neurophysiological bases of sensory predictions of "what' (predictive coding) and 'when' (predictive timing), with an emphasis on low-level oscillatory mechanisms. We argue that neural rhythms offer distinct and adapted computational solutions to predicting 'what' is going to happen in the sensory environment and 'when'.