The role of the nucleus accumbens and rostral anterior cingulate cortex in anhedonia: Integration of resting EEG, fMRI, and volumetric techniques

Wacker, Jan; Dillon, Daniel G.; Pizzagalli, Diego A.

doi:10.1016/j.neuroimage.2009.01.058

Cited by 358 publications

(273 citation statements)

References 104 publications

(173 reference statements)

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“…Furthermore, rBN subjects were unable to distinguish between negative and positive feedback in the dorsal caudate nucleus, a region implicated in linking action to outcome (Wagner et al, 2010). Critically, response bias as measured by the current task has been found to correlate with reward-related activation in striatal regions Wacker et al, 2009) and was modulated by dopaminergic challenges (Pizzagalli et al, 2008). Together with these prior findings, the current data highlight an impaired, dopaminergic-mediated tendency to modulate behavior as a function of prior reinforcements in individuals with a history of BN.…”

Section: Discussionmentioning

confidence: 63%

Dopamine-Related Deficit in Reward Learning After Catecholamine Depletion in Unmedicated, Remitted Subjects with Bulimia Nervosa

Grob

Pizzagalli

Dutra

et al. 2012

Neuropsychopharmacol

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Disturbances in reward processing have been implicated in bulimia nervosa (BN). Abnormalities in processing reward-related stimuli might be linked to dysfunctions of the catecholaminergic neurotransmitter system, but findings have been inconclusive. A powerful way to investigate the relationship between catecholaminergic function and behavior is to examine behavioral changes in response to experimental catecholamine depletion (CD). The purpose of this study was to uncover putative catecholaminergic dysfunction in remitted subjects with BN who performed a reinforcement-learning task after CD. CD was achieved by oral alpha-methyl-para-tyrosine (AMPT) in 19 unmedicated female subjects with remitted BN (rBN) and 28 demographically matched healthy female controls (HC). Sham depletion administered identical capsules containing diphenhydramine. The study design consisted of a randomized, double-blind, placebo-controlled crossover, single-site experimental trial. The main outcome measures were reward learning in a probabilistic reward task analyzed using signal-detection theory. Secondary outcome measures included self-report assessments, including the Eating Disorder Examination-Questionnaire. Relative to healthy controls, rBN subjects were characterized by blunted reward learning in the AMPTFbut not in placeboFcondition. Highlighting the specificity of these findings, groups did not differ in their ability to perceptually distinguish between stimuli. Increased CD-induced anhedonic (but not eating disorder) symptoms were associated with a reduced response bias toward a more frequently rewarded stimulus. In conclusion, under CD, rBN subjects showed reduced reward learning compared with healthy control subjects. These deficits uncover disturbance of the central reward processing systems in rBN related to altered brain catecholamine levels, which might reflect a trait-like deficit increasing vulnerability to BN.

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Section: Discussionmentioning

confidence: 63%

Dopamine-Related Deficit in Reward Learning After Catecholamine Depletion in Unmedicated, Remitted Subjects with Bulimia Nervosa

Grob

Pizzagalli

Dutra

et al. 2012

Neuropsychopharmacol

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“…Recent research on the neurobiology of major depression has also focused on the ACC. More specifically, the major depression symptom of anhedonia, characterized by reward-insensitive behavior and blunted positive emotionality -and hence, apparently, the extremely low end of aE (Depue, 1995) -has been associated with abnormally low levels of activity in the ventral-rostral ACC (rACC) regions (Pizzagalli, Peccoralo, Davidson, & Cohen, 2006) and with blunted nucleus accumbens responses to reward signals (Wacker, Dillon, & Pizzagalli, 2009). Furthermore, pharmacological challenge studies have demonstrated that the ACC responds to dopaminergic drugs (e.g., Völlm et al, 2004), and ACC activity also qualifies as a predictor for psychopharmacological treatment responses (for selective norepinephrine and serotonin reuptake inhibitors, see Korb, Hunter, Cook, & Leuchter, 2009).…”

Section: Agentic Extraversion and Anterior Cingulate Cortex Activitymentioning

confidence: 99%

Rostral anterior cingulate activity generates posterior versus anterior theta activity linked to agentic extraversion

Chavanon

Wacker

Stemmler

2010

Cogn Affect Behav Neurosci

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Recent research using the resting electroencephalogram (EEG) showed that posterior versus anterior theta activity (around 4-8 Hz) is consistently associated with agency, reflecting the dopaminergic core of extraversion (i.e., incentive motivation, positive emotion). Neuroimaging studies using various methodologies and experimental paradigms have converged on the anterior cingulate cortex (ACC) as a neurophysiological correlate of extraversion. The aim of the present study is integrate these lines of research by testing the hypothesis that posterior versus anterior EEG theta is at least partly based on ACC theta activity. Resting EEG data were analyzed in N = 78 healthy, male participants extremely high or low in agentic extraversion (aE). Using the low-resolution electromagnetic tomography algorithm, we localized the sources of aE-dependent intracerebral theta activity within rostral subdivisions of the ACC. The posterior versus anterior index and theta current density within the rostral ACC were significantly correlated (r = -.52), and both displayed high retest stability across 5 hr and were associated with traits from the aE spectrum. These neurophysiological correlates of aE and their possible functional significance are discussed.

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“…The second aim was to investigate the relationship between reward processing and nucleus accumbens volume in PCP and controls. Since anhedonia is common in PCP and interacts with both reward responsiveness (Beevers and Meyer, 2002) and nucleus accumbens volume (Harvey et al, 2007;Wacker et al, 2010), correlation analyses were corrected for anhedonia.…”

Section: Introductionmentioning

confidence: 99%

Reward responsiveness in patients with chronic pain

Elvemo

Landrø

Borchgrevink

et al. 2015

European Journal of Pain

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Background: It is proposed that changes in reward processing in the brain are involved in the pathophysiology of pain based on experimental studies. The first aim of the present study was to investigate if reward drive and/or reward responsiveness was altered in patients with chronic pain (PCP) compared to controls matched for education, age and sex. The second aim was to investigate the relationship between reward processing and nucleus accumbens volume in PCP and controls. Nucleus accumbens is central in reward processing and its structure has been shown to be affected by chronic pain conditions in previous studies. Methods: Reward drive and responsiveness were assessed with the Behavioral Inhibition Scale/Behavioral Activation Scale, and nucleus accumbens volumes obtained from T1-weighted brain MRIs obtained at 3T in 19 PCP of heterogeneous aetiologies and 20 age-, sex-and education-matched healthy controls. Anhedonia was assessed with Beck's Depression Inventory II. Results: The PCP group had significantly reduced scores on the reward responsiveness, but not reward drive. There was a trend towards smaller nucleus accumbens volume in the PCP compared to control group. There was a significant positive partial correlation between reward responsiveness and nucleus accumbens volume in the PCP group adjusted for anhedonia, which was significantly different from the same relationship in the control group. Conclusions: Reward responsiveness is reduced in chronic pain patients of heterogeneous aetiology, and this reduction was associated with nucleus accumbens volume. Reduced reward responsiveness could be a marker of chronic pain vulnerability, and may indicate reduced opioid function.

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The role of the nucleus accumbens and rostral anterior cingulate cortex in anhedonia: Integration of resting EEG, fMRI, and volumetric techniques

Cited by 358 publications

References 104 publications

Dopamine-Related Deficit in Reward Learning After Catecholamine Depletion in Unmedicated, Remitted Subjects with Bulimia Nervosa

Dopamine-Related Deficit in Reward Learning After Catecholamine Depletion in Unmedicated, Remitted Subjects with Bulimia Nervosa

Rostral anterior cingulate activity generates posterior versus anterior theta activity linked to agentic extraversion

Reward responsiveness in patients with chronic pain

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