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Dive into the research topics where Oliver J. Robinson is active.

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Featured researches published by Oliver J. Robinson.


Neuropsychopharmacology | 2008

Acute Tryptophan Depletion in Healthy Volunteers Enhances Punishment Prediction but Does not Affect Reward Prediction

Roshan Cools; Oliver J. Robinson; Barbara J. Sahakian

Central serotonin (5-HT) has been implicated in emotional and behavioral control processes for many decades, but its precise contribution is not well understood. We used the acute tryptophan depletion procedure in young healthy volunteers to test the hypothesis that central 5-HT is critical for predicting punishment. An observational reversal-learning task was employed that provided separate measures of punishment and reward prediction. Under baseline, subjects made more prediction errors for punishment-associated stimuli than for reward-associated stimuli. This bias was abolished after central 5-HT depletion, which enhanced the ability to predict punishment while not affecting reward prediction. The selective potentiation of punishment prediction concurs with recent theorizing, suggesting that central 5-HT carries a prediction error for future punishment, but not for future reward (Daw et al, 2002). Furthermore, the finding highlights the importance of central 5-HT in resilience to adversity and may have implications for a variety of neuropsychiatric disorders including depression and anxiety.


Frontiers in Human Neuroscience | 2013

The impact of anxiety upon cognition: perspectives from human threat of shock studies

Oliver J. Robinson; Katherine Vytal; Brian R. Cornwell; Christian Grillon

Anxiety disorders constitute a sizeable worldwide health burden with profound social and economic consequences. The symptoms are wide-ranging; from hyperarousal to difficulties with concentrating. This latter effect falls under the broad category of altered cognitive performance which is the focus of this review. Specifically, we examine the interaction between anxiety and cognition focusing on the translational threat of unpredictable shock paradigm; a method previously used to characterize emotional responses and defensive mechanisms that is now emerging as valuable tool for examining the interaction between anxiety and cognition. In particular, we compare the impact of threat of shock on cognition in humans to that of pathological anxiety disorders. We highlight that both threat of shock and anxiety disorders promote mechanisms associated with harm avoidance across multiple levels of cognition (from perception to attention to learning and executive function)—a “hot” cognitive function which can be both adaptive and maladaptive depending upon the circumstances. This mechanism comes at a cost to other functions such as working memory, but leaves some functions, such as planning, unperturbed. We also highlight a number of cognitive effects that differ across anxiety disorders and threat of shock. These discrepant effects are largely seen in “cold” cognitive functions involving control mechanisms and may reveal boundaries between adaptive (e.g., response to threat) and maladaptive (e.g., pathological) anxiety. We conclude by raising a number of unresolved questions regarding the role of anxiety in cognition that may provide fruitful avenues for future research.


NeuroImage | 2012

The adaptive threat bias in anxiety: amygdala- dorsomedial prefrontal cortex coupling and aversive amplification

Oliver J. Robinson; Danielle R. Charney; Cassie Overstreet; Katherine Vytal; Christian Grillon

Functionally, anxiety serves to increase vigilance towards aversive stimuli and improve the ability to detect and avoid danger. We have recently shown, for instance, that anxiety increases the ability to a) detect and b) instigate defensive responses towards aversive and not appetitive face stimuli in healthy individuals. This is arguably the key adaptive function of anxiety, yet the neural circuitry underlying this valence-specific effect is unknown. In the present translational study, we sought evidence for the proposition that dorsomedial regions of the prefrontal (DMPFC) and cingulate cortex constitute the human homologue of the rodent prelimbic and are thus associated with increased amygdala responding during this adaptive threat bias in anxiety. To this end, we applied a novel functional connectivity analysis to healthy subjects (N=20) identifying the emotion of fearful and happy faces in an fMRI scanner under anxious (threat of unpredictable foot shock) and non-anxious (safe) conditions. We showed that anxiety significantly increased positive DMPFC-amygdala connectivity during the processing of fearful faces. This effect was a) valence-specific (it was not seen for happy faces), b) paralleled by faster behavioral response to fearful faces, and c) correlated positively with trait anxiety. As such we provide the first experimental support for an anxiety-mediated, valence-specific, DMPFC-amygdala aversive amplification mechanism in healthy humans. This may be homologous to the rodent prelimbic-amygdala circuit and may, given the relationship with trait anxiety, underlie vulnerability to anxiety disorders. This study thus pinpoints a key neural mechanism in adaptive anxiety and highlights its potential link to maladaptive anxiety.


Psychopharmacology | 2012

Reliance on habits at the expense of goal-directed control following dopamine precursor depletion

Sanne de Wit; Holly R. Standing; Elise E. DeVito; Oliver J. Robinson; K. Richard Ridderinkhof; Trevor W. Robbins; Barbara J. Sahakian

RationaleDopamine is well known to play an important role in learning and motivation. Recent animal studies have implicated dopamine in the reinforcement of stimulus–response habits, as well as in flexible, goal-directed action. However, the role of dopamine in human action control is still not well understood.ObjectivesWe present the first investigation of the effect of reducing dopamine function in healthy volunteers on the balance between habitual and goal-directed action control.MethodsThe dietary intervention of acute dietary phenylalanine and tyrosine depletion (APTD) was adopted to study the effects of reduced global dopamine function on action control. Participants were randomly assigned to either the APTD or placebo group (ns = 14) to allow for a between-subjects comparison of performance on a novel three-stage experimental paradigm. In the initial learning phase, participants learned to respond to different stimuli in order to gain rewarding outcomes. Subsequently, an outcome-devaluation test and a slips-of-action test were conducted to assess whether participants were able to flexibly adjust their behaviour to changes in the desirability of the outcomes.ResultsAPTD did not prevent stimulus–response learning, nor did we find evidence for impaired response–outcome learning in the subsequent outcome-devaluation test. However, when goal-directed and habitual systems competed for control in the slips-of-action test, APTD tipped the balance towards habitual control. These findings were restricted to female volunteers.ConclusionsWe provide direct evidence that the balance between goal-directed and habitual control in humans is dopamine dependent. The results are discussed in light of gender differences in dopamine function and psychopathologies.


Cognitive, Affective, & Behavioral Neuroscience | 2011

The effect of induced anxiety on cognition: threat of shock enhances aversive processing in healthy individuals

Oliver J. Robinson; Allison M. Letkiewicz; Cassie Overstreet; Monique Ernst; Christian Grillon

Individuals with anxiety disorders demonstrate altered cognitive performance including (1) cognitive biases towards negative stimuli (affective biases) and (2) increased cognitive rigidity (e.g., impaired conflict adaptation) on affective Stroop tasks. Threat of electric shock is frequently used to induce anxiety in healthy individuals, but the extent to which this manipulation mimics the cognitive impairment seen in anxiety disorders is unclear. In this study, 31 healthy individuals completed an affective Stroop task under safe and threat-of-shock conditions. We showed that threat (1) enhanced aversive processing and abolished a positive affective bias but (2) had no effect on conflict adaptation. Threat of shock thus partially models the effects of anxiety disorders on affective Stroop tasks. We suggest that the affective state of anxiety—which is common to both threat and anxiety disorders—modulates the neural inhibition of subcortical aversive processing, whilst pathologies unique to anxiety disorders modulate conflict adaptation.


Psychological Medicine | 2008

Recurrence in major depressive disorder: a neurocognitive perspective

Oliver J. Robinson; Barbara J. Sahakian

Depressive disorders are amongst the leading causes of disability and mortality worldwide and, as such, it is predicted that by 2010 only cardio-ischaemic disorders will provide a greater burden. In addition to the sizable emotional, individual and social burden, depressive disorders cost an estimated US


NeuroImage | 2010

Dissociable responses to punishment in distinct striatal regions during reversal learning.

Oliver J. Robinson; Michael J. Frank; Barbara J. Sahakian; Roshan Cools

83.1 billion per year in the United States alone. In spite of effective treatments, a large proportion of sufferers go on to experience recurrences. With successive recurrences, the likelihood of subsequent episodes increases. Despite this, research to date has tended to focus on first episodes or else has not distinguished between episodes. This editorial review highlights a number of differences between first and recurrent episodes which, in turn, recommend more longitudinal, recurrence-oriented, treatments. We also examine the findings from acute tryptophan depletion studies which, it is speculated, help to understand the differences between successive episodes. The overall aim, however, is to highlight the importance of recurrence in depression and to stimulate debate.


Proceedings of the National Academy of Sciences of the United States of America | 2013

Stress increases aversive prediction error signal in the ventral striatum.

Oliver J. Robinson; Cassie Overstreet; Danielle R. Charney; Katherine Vytal; Christian Grillon

Adaptive behavior depends on the ability to flexibly alter our choices in response to changes in reward and punishment contingencies. One brain region frequently implicated in such behavior is the striatum. However, this region is functionally diverse and there are a number of apparent inconsistencies across previous studies. For instance, how can significant BOLD responses in the ventral striatum during punishment-based reversal learning be reconciled with the frequently demonstrated role of the ventral striatum in reward processing? Here we attempt to address this question by separately examining BOLD responses during reversal learning driven by reward and during reversal learning driven by punishment. We demonstrate simultaneous valence-specific and valence-nonspecific signals in the striatum, with the posterior dorsal striatum responding only to unexpected reward, and the anterior ventral striatum responding to both unexpected punishment as well as unexpected reward. These data help to reconcile conflicting findings from previous studies by showing that distinct regions of the striatum exhibit dissociable responses to punishment during reversal learning.


The Lancet Psychiatry | 2014

The dorsal medial prefrontal (anterior cingulate) cortex–amygdala aversive amplification circuit in unmedicated generalised and social anxiety disorders: an observational study

Oliver J. Robinson; Marissa Krimsky; Lynne Lieberman; Phillip S Allen; Katherine Vytal; Christian Grillon

From job interviews to the heat of battle, it is evident that people think and learn differently when stressed. In fact, learning under stress may have long-term consequences; stress facilitates aversive conditioning and associations learned during extreme stress may result in debilitating emotional responses in posttraumatic stress disorder. The mechanisms underpinning such stress-related associations, however, are unknown. Computational neuroscience has successfully characterized several mechanisms critical for associative learning under normative conditions. One such mechanism, the detection of a mismatch between expected and observed outcomes within the ventral striatum (i.e., “prediction errors”), is thought to be a critical precursor to the formation of new stimulus–outcome associations. An untested possibility, therefore, is that stress may affect learning via modulation of this mechanism. Here we combine a translational model of stress with a cognitive neuroimaging paradigm to demonstrate that stress significantly increases ventral striatum aversive (but not appetitive) prediction error signal. This provides a unique account of the propensity to form threat-related associations under stress with direct implications for our understanding of both normal stress and stress-related disorders.


Psychopharmacology | 2012

Tryptophan depletion disinhibits punishment but not reward prediction: implications for resilience.

Oliver J. Robinson; Roshan Cools; Barbara J. Sahakian

Summary Background In four previous studies, we have delineated the role of positive circuit coupling between the dorsal medial prefrontal (anterior cingulate) cortex and the amygdala during aversive processing in healthy people under stress. This translational circuit—the aversive amplification circuit—is thought to drive adaptive, harm-avoidant behaviour in threatening environments. We assess the role of this circuit in the pathological manifestation of anxiety disorders. Methods For this single-site study, 45 unmedicated participants (22 with generalised and/or social anxiety disorder and 23 healthy controls) were recruited via advertisements from the metropolitan area of Washington, DC (USA). People who applied to participate in the study had to pass an initial telephone screen and comprehensive screening by a clinician at the National Institutes of Health (NIH; Bethesda, MD, USA). People with a contraindicated medical disorder, past or current psychiatric disorders other than anxiety disorders, and those using psychoactive medications or illicit drugs were excluded. Eligible individuals could participate as either a healthy control or a patient, depending on diagnosis. They were asked to use a button box to complete a simple emotion identification task (fearful vs happy faces; 44 trials of each) during functional MRI at the NIH. Functional imaging analysis consisted of event-related activation analysis and psychophysiological interaction connectivity analysis of regions coupled with the amygdala during task performance. Findings A diagnosis-by-valence interaction was recorded in whole-brain amygdala connectivity within the dorsal medial prefrontal (anterior cingulate) cortex clusters identified in our previous study, driven by significantly increased circuit coupling during processing of fearful faces versus happy faces in anxious, but not healthy, participants. Importantly, and in accordance with contemporary theoretical approaches to psychiatry, circuit coupling correlated positively with self-reported anxious symptoms, which provides evidence of a continuous association between the circuit and subjective symptoms. Interpretation In this study and our previous work, we track the functional role of one neural circuit from its involvement in adaptive threat biases under stress, to its chronic engagement in anxiety disorders in the absence of experimentally induced stress. Thus, we uniquely map a mood and anxiety-related circuit across its adaptive and maladaptive stages. Clinically, this study could provide a step towards a more mechanistic continuum-based approach to anxiety disorder diagnosis and might ultimately lead to more targeted treatments for patients with anxiety disorders. Funding National Institute of Mental Health, USA, and Medical Research Council

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Christian Grillon

National Institutes of Health

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Cassie Overstreet

National Institutes of Health

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Katherine Vytal

National Institutes of Health

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Jessica Aylward

University College London

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Monique Ernst

National Institutes of Health

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Roshan Cools

Radboud University Nijmegen

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Sarah Peters

University College London

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