The Brain’s Response to Reward Anticipation and Depression in Adolescence: Dimensionality, Specificity, and Longitudinal Predictions in a Community-Based Sample

Stringaris, Argyris; Vidal‐Ribas, Pablo; Artiges, Éric; Lemaître, Hervé; Gollier-Briant, Fanny; Wolke, Selina; Vulser, Hélène; Miranda, Rubén; Penttilä, Jani; Struve, Maren; Fadai, Tahmine; Kappel, Viola; Grimmer, Yvonne; Goodman, Robert; Poustka, Luise; Conrod, Patricia J.; Cattrell, Anna; Banaschewski, Tobias; Bokde, Arun L.W.; Bromberg, Uli; Büchel, Christian; Flor, Herta; Frouin, Vincent; Gallinat, Juergen; Garavan, Hugh; Gowland, Penny; Heinz, Andreas; Ittermann, Bernd; Nees, Frauke; Papadopoulos, Dimitri; Paus, Tomáš; Smolka, Michael N.; Walter, Henrik; Whelan, Robert; Martinot, Jean‐Luc; Schumann, Günter; Paillère-Martinot, Marie-Laure

doi:10.1176/appi.ajp.2015.14101298

Cited by 260 publications

(224 citation statements)

References 37 publications

(33 reference statements)

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“…These latter approaches have been mostly consistent in their observation of blunted striatal responses to reward outcomes or reward-predicting cues in MDD patients (Dichter et al, 2009;Forbes et al, 2009;Gotlib et al, 2010;Pizzagalli et al, 2009), and these initial findings have been replicated in recent studies with larger patient samples. Indeed, one recent study of over 1500 adolescents found that reduced ventral striatal activity during reward anticipation was associated with clinical or subclinical depression, and that lower ventral striatal activity in non-depressed teens at the time of scanning was predictive of developing depressive symptoms over a 2-year follow-up period (Stringaris et al, 2015). In addition to neural responses to anticipation, a second recent study identified a failure in the expected temporal shift of striatal responses to reward cues from reward outcomes as a task was learned, a pattern that was specific to patients with greater anhedonia (Greenberg et al, 2015).…”

Section: Reduced Motivation and Psychomotor Function In Psychiatric Dmentioning

confidence: 99%

Inflammation Effects on Motivation and Motor Activity: Role of Dopamine

Felger

Treadway

2016

Neuropsychopharmacol

303

237

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Motivational and motor deficits are common in patients with depression and other psychiatric disorders, and are related to symptoms of anhedonia and motor retardation. These deficits in motivation and motor function are associated with alterations in corticostriatal neurocircuitry, which may reflect abnormalities in mesolimbic and mesostriatal dopamine (DA). One pathophysiologic pathway that may drive changes in DAergic corticostriatal circuitry is inflammation. Biomarkers of inflammation such as inflammatory cytokines and acute-phase proteins are reliably elevated in a significant proportion of psychiatric patients. A variety of inflammatory stimuli have been found to preferentially target basal ganglia function to lead to impaired motivation and motor activity. Findings have included inflammation-associated reductions in ventral striatal neural responses to reward anticipation, decreased DA and DA metabolites in cerebrospinal fluid, and decreased availability, and release of striatal DA, all of which correlated with symptoms of reduced motivation and/or motor retardation. Importantly, inflammation-associated symptoms are often difficult to treat, and evidence suggests that inflammation may decrease DA synthesis and availability, thus circumventing the efficacy of standard pharmacotherapies. This review will highlight the impact of administration of inflammatory stimuli on the brain in relation to motivation and motor function. Recent data demonstrating similar relationships between increased inflammation and altered DAergic corticostriatal circuitry and behavior in patients with major depressive disorder will also be presented. Finally, we will discuss the mechanisms by which inflammation affects DA neurotransmission and relevance to novel therapeutic strategies to treat reduced motivation and motor symptoms in patients with high inflammation.

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Section: Reduced Motivation and Psychomotor Function In Psychiatric Dmentioning

confidence: 99%

Inflammation Effects on Motivation and Motor Activity: Role of Dopamine

Felger

Treadway

2016

Neuropsychopharmacol

303

237

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“…A promising pathophysiological mechanism in depression is that of sensitivity to losses and rewards, with some studies showing either reduced reactivity to rewards (1), or increased reactivity to losses (2, 3), or reduced reactivity to rewards and losses (4). Importantly, studies show that these alterations in reward reactivity are evident in children and adolescents at high risk for developing depression (5, 6) and prospectively predict worsening of depression symptoms (7–9). However, research on neural correlates of loss or reward sensitivity in adolescent depression is limited in that it has focused almost exclusively on reward sensitivity as well as striatal mechanisms that support it (1, 5).…”

Section: Introductionmentioning

confidence: 99%

Orbitofrontal Cortex Activity and Connectivity Predict Future Depression Symptoms in Adolescence

Jin

Narayanan

Luking

et al. 2017

Biological Psychiatry: Cognitive Neuroscience and Neuroimaging

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Background Major depressive disorder is a leading cause of disability worldwide; however, little is known about pathological mechanisms involved in its development. Research in adolescent depression has focused on reward sensitivity and striatal mechanisms implementing it. The contribution of loss sensitivity to future depression, as well as the orbitofrontal cortex (OFC) mechanisms critical for processing losses and rewards, remain unexplored. Furthermore, it is unclear whether OFC functioning interacts with familial history in predicting future depression. Methods In this longitudinal study we recorded functional magnetic resonance imaging (fMRI) data while 229 adolescent females with or without parental history of depression completed a monetary gambling task. We examined if OFC blood-oxygen-level-dependent (BOLD) response and functional connectivity during loss and win feedback was associated with depression symptoms concurrently and prospectively (9 months later), and whether this relationship was moderated by parental history of depression. Results Reduced OFC response during loss was associated with higher depression symptoms concurrently and prospectively, even after controlling for concurrent depression, specifically in adolescents with parental history of depression. Similarly, increased OFC-posterior insula connectivity during loss was associated with future depression symptoms but this relationship was not moderated by parental history of depression. Conclusions This study provides the first evidence for loss-related alterations in OFC functioning and its interaction with familial history of depression as possible mechanisms in the development of depression. While the current fMRI literature has mainly focused on reward, the present findings underscore the need to include prefrontal loss processing in existing developmental models of depression.

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“…15,21 However, on a meta-analytic level including studies with unmedicated and medicated patients the association of neural alterations during reward processing and positive symptoms is less clearly delineated. 24 Furthermore, the association between striatal dysfunction and depressive symptoms is well described within depressive disorders 28,29 but data are limited for schizophrenia. 30,31 Most research did not take into account the neural basis of symptom dimensions on a psychosis continuum with broadly defined first-episode psychosis patients or individuals with schizotypal personality traits (SPT).…”

Section: Introductionmentioning

confidence: 99%

Ventral Striatal Dysfunction and Symptom Expression in Individuals With Schizotypal Personality Traits and Early Psychosis

Kirschner

Hager

Muff

et al. 2016

SCHBUL

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Striatal abnormalities play a crucial role in the pathophysiology of schizophrenia. Growing evidence suggests an association between aberrant striatal activity during reward anticipation and symptom dimensions in schizophrenia. However, it is not clear whether this holds across the psychosis continuum. The aim of the present study was to investigate alterations of ventral striatal activation during reward anticipation and its relationship to symptom expression in persons with schizotypal personality traits (SPT) and first-episode psychosis. Twenty-six individuals with high SPT, 26 patients with non-affective first-episode psychosis (including 13 with brief psychotic disorder (FEP-BPD) and 13 with first-episode schizophrenia [FEP-SZ]) and 25 healthy controls underwent event-related functional magnetic resonance imaging while performing a variant of the Monetary Incentive Delay task. Ventral striatal activation was positively correlated with total symptom severity, in particular with levels of positive symptoms. This association was observed across the psychosis continuum and within each subgroup. Patients with FEP-SZ showed the strongest elevation of striatal activation during reward anticipation, although symptom levels did not differ between groups in the psychosis continuum. While our results provide evidence that variance in striatal activation is mainly explained by dimensional symptom expression, patients with schizophrenia show an additional dysregulation of striatal activation. Trans-diagnostic approaches are promising in order to disentangle dimensional and categorical neural mechanisms in the psychosis continuum.

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The Brain’s Response to Reward Anticipation and Depression in Adolescence: Dimensionality, Specificity, and Longitudinal Predictions in a Community-Based Sample

Cited by 260 publications

References 37 publications

Inflammation Effects on Motivation and Motor Activity: Role of Dopamine

Inflammation Effects on Motivation and Motor Activity: Role of Dopamine

Orbitofrontal Cortex Activity and Connectivity Predict Future Depression Symptoms in Adolescence

Ventral Striatal Dysfunction and Symptom Expression in Individuals With Schizotypal Personality Traits and Early Psychosis

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