Antidepressant drug administration modulates emotional processing in depressed patients very early in treatment, before changes occur in mood and symptoms. This effect may ameliorate the negative biases in information processing that characterize mood and anxiety disorders. It also suggests a mechanism of action compatible with cognitive theories of depression.

Anxiety patients exhibit attentional biases toward threat, which have often been demonstrated as increased distractibility by threatening stimuli. In contrast, speeded detection of threat has rarely been shown. Therefore, the authors studied both phenomena in 3 versions of a visual search task while eye movements were recorded continuously. Spider-fearful individuals and nonanxious control participants participated in a target search task, an odd-one-out search task, and a category search task. Evidence for disorder-specific increased distraction by threat was found in all tasks, whereas speeded threat detection did not occur in the target search task. The implications of these findings for cognitive theories of anxiety are discussed, particularly in relation to the concept of disengagement from threat.

Seven experiments explore the role of bottlenecks in selective attention and access to visual shortterm memory in the failure of observers to identify clearly visible changes in otherwise stable visual displays. Experiment One shows that observers fail to register a color change in an object even if they are cued to the location of the object by a transient at that location as the change is occurring. Experiment Two shows the same for orientation change. In Experiments Three and Four, attention is directed to specific objects prior to making changes in those objects. Observers have only a very limited memory for the status of recently attended items. Experiment Five reveals that observers have no ability to detect changes that happen after attention has been directed to an object and before attention returns to that object. In Experiment Six, attention is cued at rates that more closely resemble natural rates and Experiment Seven uses natural images. Memory capacity remains very small (<4 items).If you ask typical observers, outside of a vision research laboratory, what they are seeing right now, they will probably tell you that they are seeing a large number of objects placed in a spatially continuous scene. If you ask them if they are seeing all of that at the same time, they will look at you quizzically but they will agree that all of the objects seem to be visually present in the present instant of time. It hardly seems like much of a question. However, if you ask atypical observers, those who have been studying the question over the past 20 years or so, the answers may be quite different. A range of phenomena suggest that human observers are unable to perform tasks that would seem to be quite trivial if we could see what was in front of our eyes in the uncomplicated manner suggested by naïve introspection.Change blindness is one of the most striking of these phenomena. In a typical change blindness paradigm, the observer is told to monitor an image for a change. As long as transients are masked and as long as the observer is not attending to the object that is changing, observers will be very poor at detecting quite substantial changes. These can range from changes to significant objects in natural scenes to changes in "basic features" like color (Phillips, 1974;Rensink, O'Regan, & Clark, 1997;Simons, 2000;Simons & Levin, 1997).Similar failures to report what is in front of the eyes occur when observers are attending to one aspect of a display and subsequently queried about another. Thus, Mack and Rock (1998) found that observers who were answering a question about a pair of lines would fail to report salient stimuli presented at fixation ("inattentional blindness"). Simons Neisser & Becklen, 1975) have shown that observers who were monitoring one set of actors would fail to notice other actors (e.g. a woman in a gorilla suit) as they entered and left a scene (Simons & Chabris, 1999).Some have argued that these results demonstrate that we only "see" the current object of attention and that the re...

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These results suggest that 7 days of SSRI administration can increase neural markers of fear reactivity in subjects at the high end of the N dimension and may be related to early increases in anxiety and agitation seen early in treatment. Such processes may be involved in the later therapeutic effects through decreased avoidance and increased learning about social 'threat' cues.

Background: Exposure therapy is a first-line treatment for anxiety disorders but remains ineffective in a large proportion of patients. A proposed mechanism of exposure involves inhibitory learning where the association between a stimulus and an aversive outcome is suppressed by a new association with an appetitive or neutral outcome. The blood pressure medication losartan augments fear extinction in rodents and might have similar synergistic effects on human exposure therapy, but the exact cognitive mechanisms underlying these effects remain unknown.Methods: We used a reinforcement learning paradigm with compound rewards and punishments to test the prediction that losartan augments learning from appetitive relative to aversive outcomes. In a double-blind parallel design, healthy volunteers were randomly assigned to single-dose losartan (50mg) (N=28) versus placebo (N=25). Participants then performed a reinforcement learning task which simultaneously probes appetitive and aversive learning. Participant choice behaviour was analysed using both a standard reinforcement learning model and analysis of choice switching behaviour.Results: Losartan significantly reduced learning rates from aversive events (losses) when participants were first exposed to the novel task environment, while preserving learning from positive outcomes. The same effect was seen in choice switching behaviour. Conclusion:This study shows that losartan enhances learning from positive relative to negative events. This effect may represent a computationally defined neurocognitive mechanism by which the drug could enhance the effect of exposure in clinical populations.

Neuroimaging studies in anorexia nervosa (AN) suggest that altered food reward processing may result from dysfunction in both limbic reward and cortical control centers of the brain. This fMRI study aimed to index the neural correlates of food reward in a subsample of individuals with restrictive AN: twelve currently ill, fourteen recovered individuals and sixteen healthy controls. Participants were shown pictures of high and low-calorie foods and asked to evaluate how much they wanted to eat each one following a four hour fast. Whole-brain task-activated analysis was followed by psychophysiological interaction analysis (PPI) of the amygdala and caudate. In the AN group, we observed a differential pattern of activation in the lateral frontal pole: increasing following presentation of high-calorie stimuli and decreasing in during presentation of low-calorie food pictures, the opposite of which was seen in the healthy control (HC) group. In addition, decreased activation to food pictures was observed in somatosensory regions in the AN group. PPI analyses suggested hypo-connectivity in reward pathways, and between the caudate and both somatosensory and visual processing regions in the AN group. No significant between-group differences were observed between the recovered group and the currently ill and healthy controls in the PPI analysis. Taken together, these findings further our understanding of the neural processes which may underpin the avoidance of high-calorie foods in those with AN and might exacerbate the development of compulsive weight-loss behavior, despite emaciation.

Impairments in emotion regulation are thought to have a key role in the pathogenesis of anxiety disorders, but the neurobiological underpinnings contributing to vulnerability remain poorly understood. It has been a long-held view that exaggerated fear is linked to hyperresponsivity of limbic brain areas and impaired recruitment of prefrontal control. However, increasing evidence suggests that prefrontal–cortical networks are hyperactive during threat processing in anxiety disorders. This study directly explored limbic–prefrontal neural response, connectivity and heart-rate variability (HRV) in patients with a severe anxiety disorder during incidental versus intentional emotion regulation. During 3 Tesla functional magnetic resonance imaging, 18 participants with panic disorder and 18 healthy controls performed an emotion regulation task. They either viewed negative images naturally (Maintain), or they were instructed to intentionally downregulate negative affect using previously taught strategies of cognitive reappraisal (Reappraisal). Electrocardiograms were recorded throughout to provide a functional measure of regulation and emotional processing. Compared with controls, patients showed increased neural activation in limbic–prefrontal areas and reduced HRV during incidental emotion regulation (Maintain). During intentional regulation (Reappraisal), group differences were significantly attenuated. These findings emphasize patients' ability to regulate negative affect if provided with adaptive strategies. They also bring prefrontal hyperactivation forward as a potential mechanism of psychopathology in anxiety disorders. Although these results challenge models proposing impaired allocation of prefrontal resources as a key characteristic of anxiety disorders, they are in line with more recent neurobiological frameworks suggesting that prefrontal hyperactivation might reflect increased utilisation of maladaptive regulation strategies quintessential for anxiety disorders.