Intact striatal dopaminergic modulation of reward learning and daily-life reward-oriented behavior in first-degree relatives of individuals with psychotic disorder

2017 ◽  
Vol 48 (11) ◽  
pp. 1909-1914 ◽  
Author(s):  
Zuzana Kasanova ◽  
Jenny Ceccarini ◽  
Michael J. Frank ◽  
Thérèse van Amelsvoort ◽  
Jan Booij ◽  
...  
Keyword(s):  
Reinforcement Learning ◽  
Psychotic Disorders ◽  
Daily Life ◽  
Familial Risk ◽  
Reward Processing ◽  
Reward Learning ◽  
Familial Predisposition ◽  
First Degree Relatives ◽  
Dopaminergic Modulation ◽  
Da Release

BackgroundAbnormalities in reward learning in psychotic disorders have been proposed to be linked to dysregulated subcortical dopaminergic (DA) neurotransmission, which in turn is a suspected mechanism for predisposition to psychosis. We therefore explored the striatal dopaminergic modulation of reward processing and its behavioral correlates in individuals at familial risk for psychosis.MethodsWe performed a DA D2/3 receptor [18F]fallypride positron emission tomography scan during a probabilistic reinforcement learning task in 16 healthy first-degree relatives of patients with psychosis and 16 healthy volunteers, followed by a 6-day ecological momentary assessment study capturing reward-oriented behavior in the everyday life.ResultsWe detected significant reward-induced DA release in bilateral caudate, putamen and ventral striatum of both groups, with no group differences in its magnitude nor spatial extent. In both groups alike, greater extent of reward-induced DA release in all regions of interest was associated with better performance in the task, as well as in greater tendency to be engaged in reward-oriented behavior in the daily life.ConclusionsThese findings suggest intact striatal dopaminergic modulation of reinforcement learning and reward-oriented behavior in individuals with familial predisposition to psychosis. Furthermore, this study points towards a key link between striatal reward-related DA release and pursuit of ecologically relevant rewards.

Daily-life stress differentially impacts ventral striatal dopaminergic modulation of reward processing in first-degree relatives of individuals with psychosis

2018 ◽  
Vol 28 (12) ◽  
pp. 1314-1324 ◽  
Author(s):  
Zuzana Kasanova ◽  
Jenny Ceccarini ◽  
Michael J Frank ◽  
Thérèse van Amelsvoort ◽  
Jan Booij ◽  
...  
Keyword(s):  
Life Stress ◽  
Daily Life ◽  
Reward Processing ◽  
First Degree Relatives ◽  
Dopaminergic Modulation

scholarly journals Comparison of conventional and rapid-acting antidepressants in a rodent probabilistic reversal learning task

2020 ◽  
Vol 4 ◽  
pp. 239821282090717 ◽  
Author(s):  
Matthew P. Wilkinson ◽  
John P. Grogan ◽  
Jack R. Mellor ◽  
Emma S. J. Robinson
Keyword(s):  
Reinforcement Learning ◽  
Reversal Learning ◽  
Antidepressant Treatment ◽  
Learning Task ◽  
Reward Processing ◽  
Reward Learning ◽  
Feedback Sensitivity ◽  
Rule Changes ◽  
Reinforcement Learning Model ◽  
Probabilistic Reversal Learning

Deficits in reward processing are a central feature of major depressive disorder with patients exhibiting decreased reward learning and altered feedback sensitivity in probabilistic reversal learning tasks. Methods to quantify probabilistic learning in both rodents and humans have been developed, providing translational paradigms for depression research. We have utilised a probabilistic reversal learning task to investigate potential differences between conventional and rapid-acting antidepressants on reward learning and feedback sensitivity. We trained 12 rats in a touchscreen probabilistic reversal learning task before investigating the effect of acute administration of citalopram, venlafaxine, reboxetine, ketamine or scopolamine. Data were also analysed using a Q-learning reinforcement learning model to understand the effects of antidepressant treatment on underlying reward processing parameters. Citalopram administration decreased trials taken to learn the first rule and increased win-stay probability. Reboxetine decreased win-stay behaviour while also decreasing the number of rule changes animals performed in a session. Venlafaxine had no effect. Ketamine and scopolamine both decreased win-stay probability, number of rule changes performed and motivation in the task. Insights from the reinforcement learning model suggested that reboxetine led animals to choose a less optimal strategy, while ketamine decreased the model-free learning rate. These results suggest that reward learning and feedback sensitivity are not differentially modulated by conventional and rapid-acting antidepressant treatment in the probabilistic reversal learning task.

Striatal dopaminergic modulation of reinforcement learning predicts reward—oriented behavior in daily life

2017 ◽  
Vol 127 ◽  
pp. 1-9 ◽  
Author(s):  
Zuzana Kasanova ◽  
Jenny Ceccarini ◽  
Michael J. Frank ◽  
Thérèse van Amelsvoort ◽  
Jan Booij ◽  
...  
Keyword(s):  
Reinforcement Learning ◽  
Daily Life ◽  
Dopaminergic Modulation

scholarly journals MMN amplitude in first-degree relatives of psychotic disorders: Links with cognition and schizotypy

2020 ◽  
Author(s):  
Kayla R. Donaldson ◽  
Emmett M. Larsen ◽  
Katherine Jonas ◽  
Sara Tramazzo ◽  
Greg Perlman ◽  
...  
Keyword(s):  
Mismatch Negativity ◽  
Healthy Subjects ◽  
Psychotic Disorders ◽  
Clinical Symptoms ◽  
Cognitive Impairments ◽  
Familial Risk ◽  
First Degree Relatives ◽  
Per Se ◽  
Meta Analyses ◽  
Schizotypal Symptoms

Background: Mismatch negativity (MMN) amplitude is reliably reduced in psychotic disorders. While several studies have examined this effect in first-degree relatives of individuals with schizophrenia, few have sought to quantify deficits in relatives of individuals with other psychotic disorders. While some studies conclude that, compared to healthy subjects, first-degree relatives of schizophrenia show reduced MMN, others contradict this finding, a discrepancy which extends to two recent meta-analyses. Furthermore, though MMN is often shown to be associated with cognitive impairments and clinical symptoms in psychotic disorders, to our knowledge no studies have sought to examine these relationships in studies of first-degree relatives. Method: The present study sought to clarify the extent of MMN amplitude reductions in a large sample of siblings of individuals with diverse psychotic disorders (n=65), compared to cases with psychosis (n=220) and never psychotic comparison subjects (n=252). We further examined associations of MMN amplitude with cognition and schizotypal symptoms across these groups. Results: We found that MMN amplitude was intact in siblings compared to cases with psychosis. MMN amplitude was associated with cognition and schizotypal symptoms dimensionally across levels of familial risk. Conclusions: The present results imply that MMN amplitude reductions emerge as a result of, or in conjunction with, clinical features associated with psychosis. Such findings carry important implications for the utility of MMN amplitude as an indicator of inherited risk, and suggest that this component may be best conceptualized as a marker for clinical symptoms and cognitive impairments, rather than risk for psychosis per se.

Neurobiological Reward-Related Abnormalities Across Mood Disorders

2019 ◽  
pp. 222-238
Author(s):  
Alexis E. Whitton ◽  
Michael T. Treadway ◽  
Manon L. Ironside ◽  
Diego A. Pizzagalli
Keyword(s):  
Decision Making ◽  
Mood Disorders ◽  
Treatment Strategies ◽  
Reward Processing ◽  
Reward Learning ◽  
Symptom Presentation ◽  
Psychiatric Symptomatology ◽  
Symptom Dimensions ◽  
Psychotherapeutic Interventions ◽  
Primary Focus

This chapter provides a critical review of recent behavioral and neuroimaging evidence of reward processing abnormalities in mood disorders. The primary focus is on the neural mechanisms underlying disruption in approach motivation, reward learning, and reward-based decision-making in major depression and bipolar disorder. Efforts focused on understanding how reward-related impairments contribute to psychiatric symptomatology have grown substantially in recent years. This has been driven by significant advances in the understanding of the neurobiology of reward processing and a growing recognition that disturbances in motivation and hedonic capacity are poorly targeted by current pharmacological and psychotherapeutic interventions. As a result, numerous studies have sought to test the presence of reward circuit dysfunction in psychiatric disorders that are marked by anhedonia, amotivation, mania, and impulsivity. Moreover, as the field has increasingly eschewed categorical diagnostic boundaries in favor of symptom dimensions, there has been a parallel rise in studies seeking to identify transdiagnostic neural markers of reward processing dysfunction that may transcend disorders. The thesis of this chapter is twofold: First, evidence indicates that specific subcomponents of reward processing map onto partially distinct neurobiological pathways. Second, specific subcomponents of reward processing, including reward learning and effort-based decision-making, are impaired across different mood disorder diagnoses and may point to dimensions in symptom presentation that possess more reliable behavioral and neural correlates. The potential for these findings to inform the development of prevention and treatment strategies is discussed.

scholarly journals Cannabinoids, reward processing, and psychosis

2021 ◽  
Author(s):  
Brandon Gunasekera ◽  
Kelly Diederen ◽  
Sagnik Bhattacharyya
Keyword(s):  
Psychotic Disorders ◽  
Neural Substrates ◽  
Brain Regions ◽  
Reward Processing ◽  
Anterior Cingulate ◽  
Psychotic Symptoms ◽  
Dopamine Synthesis ◽  
Future Research ◽  
Drug Challenge ◽  
Psychotomimetic Effects

Abstract Background Evidence suggests that an overlap exists between the neurobiology of psychotic disorders and the effects of cannabinoids on neurocognitive and neurochemical substrates involved in reward processing. Aims We investigate whether the psychotomimetic effects of delta-9-tetrahydrocannabinol (THC) and the antipsychotic potential of cannabidiol (CBD) are underpinned by their effects on the reward system and dopamine. Methods This narrative review focuses on the overlap between altered dopamine signalling and reward processing induced by cannabinoids, pre-clinically and in humans. A systematic search was conducted of acute cannabinoid drug-challenge studies using neuroimaging in healthy subjects and those with psychosis Results There is evidence of increased striatal presynaptic dopamine synthesis and release in psychosis, as well as abnormal engagement of the striatum during reward processing. Although, acute THC challenges have elicited a modest effect on striatal dopamine, cannabis users generally indicate impaired presynaptic dopaminergic function. Functional MRI studies have identified that a single dose of THC may modulate regions involved in reward and salience processing such as the striatum, midbrain, insular, and anterior cingulate, with some effects correlating with the severity of THC-induced psychotic symptoms. CBD may modulate brain regions involved in reward/salience processing in an opposite direction to that of THC. Conclusions There is evidence to suggest modulation of reward processing and its neural substrates by THC and CBD. Whether such effects underlie the psychotomimetic/antipsychotic effects of these cannabinoids remains unclear. Future research should address these unanswered questions to understand the relationship between endocannabinoid dysfunction, reward processing abnormalities, and psychosis.

Mismatch negativity amplitude in first-degree relatives of individuals with psychotic disorders: Links with cognition and schizotypy

2021 ◽  
Vol 238 ◽  
pp. 161-169
Author(s):  
Kayla R. Donaldson ◽  
Emmett M. Larsen ◽  
Katherine Jonas ◽  
Sara Tramazzo ◽  
Greg Perlman ◽  
...  
Keyword(s):  
Mismatch Negativity ◽  
Psychotic Disorders ◽  
First Degree Relatives

Emotional cognition subgroups in unaffected first-degree relatives of patients with mood disorders

2021 ◽  
pp. 1-11
Author(s):  
Hanne Lie Kjærstad ◽  
Cristina Varo ◽  
Iselin Meluken ◽  
Eduard Vieta ◽  
Maj Vinberg ◽  
...  
Keyword(s):  
Mood Disorders ◽  
Familial Risk ◽  
Hierarchical Cluster ◽  
Expression Recognition ◽  
Neurocognitive Performance ◽  
Cognitive Markers ◽  
First Degree Relatives ◽  
Probe Test ◽  
Data Driven Approach ◽  
Emotional Cognition

Abstract Background Patients with major depressive disorder (MDD) or bipolar disorder (BD) exhibit difficulties with emotional cognition even during remission. There is evidence for aberrant emotional cognition in unaffected relatives of patients with these mood disorders, but studies are conflicting. We aimed to investigate whether emotional cognition in unaffected first-degree relatives of patients with mood disorders is characterised by heterogeneity using a data-driven approach. Methods Data from 94 unaffected relatives (33 of MDD patients; 61 of BD patients) and 203 healthy controls were pooled from two cohort studies. Emotional cognition was assessed with the Social Scenarios Test, Facial Expression Recognition Test and Faces Dot-Probe Test. Hierarchical cluster analysis was conducted using emotional cognition data from the 94 unaffected relatives. The resulting emotional cognition clusters and controls were compared for emotional and non-emotional cognition, demographic characteristics and functioning. Results Two distinct clusters of unaffected relatives were identified: a relatively ‘emotionally preserved’ cluster (55%; 40% relatives of MDD probands) and an ‘emotionally blunted’ cluster (45%; 29% relatives of MDD probands). ‘Emotionally blunted’ relatives presented with poorer neurocognitive performance (global cognition p = 0.010), heightened subsyndromal mania symptoms (p = 0.004), lower years of education (p = 0.004) and difficulties with interpersonal functioning (p = 0.005) than controls, whereas ‘emotionally preserved’ relatives were comparable to controls on these measures. Conclusions Our findings show discrete emotional cognition profiles that occur across healthy first-degree relatives of patients with MDD and BD. These emotional cognition clusters may provide insight into emotional cognitive markers of genetically distinct subgroups of individuals at familial risk of mood disorders.

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