Erratum: The brain reward circuitry in mood disorders

Russo, Scott J.; Nestler, Eric J.

doi:10.1038/nrn3589

Cited by 8 publications

(2 citation statements)

References 38 publications

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“…Abnormalities in neural reward circuitry may be a key feature underlying depressive disorders, particularly the core symptom of anhedonia (Naranjo, Tremblay, & Busto, 2001; Russo & Nestler, 2013). Functional MRI (fMRI) studies have shown that, compared with healthy controls, adults with depression exhibit reduced activation to rewards in striatal regions of the brain and are less likely to adjust their behavior in response to rewards (Eshel & Roiser, 2010; Henriques & Davidson, 2000; Pizzagalli et al, 2009; Pizzagalli, Jahn, & O’Shea, 2005; Smoski et al, 2009; Steele, Kumar, & Ebmeier, 2007).…”

mentioning

confidence: 99%

Neural reactivity to rewards and losses in offspring of mothers and fathers with histories of depressive and anxiety disorders.

Kujawa

Proudfit

Klein

2014

Journal of Abnormal Psychology

141

151

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Depression appears to be characterized by reduced neural reactivity to receipt of reward. Despite evidence of shared etiologies and high rates of comorbidity between depression and anxiety, this abnormality may be relatively specific to depression. However, it is unclear whether children at risk for depression also exhibit abnormal reward responding, and if so, whether risk for anxiety moderates this association. The feedback negativity (FN) is an event-related potential component sensitive to receipt of rewards versus losses that is reduced in depression. Using a large community sample (N=407) of 9-year old children who had never experienced a depressive episode, we examined whether histories of depression and anxiety in their parents were associated with the FN following monetary rewards and losses. Results indicated that maternal history of depression was associated with a blunted FN in offspring, but only when there was no maternal history of anxiety. In addition, greater severity of maternal depression was associated with greater blunting of the FN in children. No effects of paternal psychopathology were observed. Results suggest that blunted reactivity to rewards versus losses may be a vulnerability marker that is specific to pure depression, but is not evident when there is also familial risk for anxiety. In addition, these findings suggest that abnormal reward responding is evident as early as middle childhood, several years prior to the sharp increase in the prevalence of depression and rapid changes in neural reward circuitry in adolescence.

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mentioning

confidence: 99%

Neural reactivity to rewards and losses in offspring of mothers and fathers with histories of depressive and anxiety disorders.

Kujawa

Proudfit

Klein

2014

Journal of Abnormal Psychology

141

151

View full text Add to dashboard Cite

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“…Disruptions in reward pathways of the brain have been associated with mood and anxiety disorders (Ulrich-Lai et al, 2010;Russo and Nestler, 2013). Atypical responses to pleasurable stimuli such as food or positive social interaction might be an indication of dysfunctional reward signaling which could be a sign of mood or anxiety disorders, as summarized in this section.…”

Section: Responses To Appetitive Stimulimentioning

confidence: 97%

Larval Zebrafish as a Model for Mechanistic Discovery in Mental Health

Tan

Ang

Wee

2022

Front. Mol. Neurosci.

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Animal models are essential for the discovery of mechanisms and treatments for neuropsychiatric disorders. However, complex mental health disorders such as depression and anxiety are difficult to fully recapitulate in these models. Borrowing from the field of psychiatric genetics, we reiterate the framework of ‘endophenotypes’ – biological or behavioral markers with cellular, molecular or genetic underpinnings – to reduce complex disorders into measurable behaviors that can be compared across organisms. Zebrafish are popular disease models due to the conserved genetic, physiological and anatomical pathways between zebrafish and humans. Adult zebrafish, which display more sophisticated behaviors and cognition, have long been used to model psychiatric disorders. However, larvae (up to 1 month old) are more numerous and also optically transparent, and hence are particularly suited for high-throughput screening and brain-wide neural circuit imaging. A number of behavioral assays have been developed to quantify neuropsychiatric phenomena in larval zebrafish. Here, we will review these assays and the current knowledge regarding the underlying mechanisms of their behavioral readouts. We will also discuss the existing evidence linking larval zebrafish behavior to specific human behavioral traits and how the endophenotype framework can be applied. Importantly, many of the endophenotypes we review do not solely define a diseased state but could manifest as a spectrum across the general population. As such, we make the case for larval zebrafish as a promising model for extending our understanding of population mental health, and for identifying novel therapeutics and interventions with broad impact.

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Neural correlates of emotional valence processing in Parkinson’s disease: dysfunction in the subcortex

Bell

Gilat

Shine

et al. 2017

Brain Imaging and Behavior

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Parkinson's disease (PD) is frequently accompanied by cognitive and neuropsychiatric symptoms including impairments in affective processing. Despite this, mechanisms underlying vulnerability to deficits in affective processing remain unclear. In this study, we utilized functional Magnetic Resonance Imaging (fMRI) and an Affective Go-NoGo paradigm, to examine the neural correlates of emotional valence processing in PD. Results suggest that PD is associated with aberrant processing of emotional valence in subcortical limbic structures. Specifically, we found significant group-by-valence interactions in the ventral striatum and amygdala in response to words of differing emotional valence. Our findings contribute to a broader understanding of affective processing in PD and may provide insights into the mechanisms underlying vulnerability to mood disorders in PD.

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Erratum: The brain reward circuitry in mood disorders

Cited by 8 publications

References 38 publications

Neural reactivity to rewards and losses in offspring of mothers and fathers with histories of depressive and anxiety disorders.

Neural reactivity to rewards and losses in offspring of mothers and fathers with histories of depressive and anxiety disorders.

Larval Zebrafish as a Model for Mechanistic Discovery in Mental Health

Neural correlates of emotional valence processing in Parkinson’s disease: dysfunction in the subcortex

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