Literature DB >> 22491353

Dopamine-related deficit in reward learning after catecholamine depletion in unmedicated, remitted subjects with bulimia nervosa.

Simona Grob1, Diego A Pizzagalli, Sunny J Dutra, Jair Stern, Hanspeter Mörgeli, Gabriella Milos, Ulrich Schnyder, Gregor Hasler.   

Abstract

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 AMPT--but not in placebo--condition. 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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Year:  2012        PMID: 22491353      PMCID: PMC3376326          DOI: 10.1038/npp.2012.41

Source DB:  PubMed          Journal:  Neuropsychopharmacology        ISSN: 0893-133X            Impact factor:   7.853


  53 in total

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  14 in total

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Journal:  J Neurosci       Date:  2015-06-03       Impact factor: 6.167

Review 3.  Reward Learning Through the Lens of RDoC: a Review of Theory, Assessment, and Empirical Findings in the Eating Disorders.

Authors:  Lauren M Schaefer; Joanna E Steinglass
Journal:  Curr Psychiatry Rep       Date:  2021-01-02       Impact factor: 5.285

4.  Anhedonia in Eating Disorders.

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5.  Probabilistic Reinforcement Learning and Anhedonia.

Authors:  Brian D Kangas; Andre Der-Avakian; Diego A Pizzagalli
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Review 6.  Does a shared neurobiology for foods and drugs of abuse contribute to extremes of food ingestion in anorexia and bulimia nervosa?

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Journal:  Biol Psychiatry       Date:  2013-02-04       Impact factor: 13.382

7.  Dopamine depletion attenuates some behavioral abnormalities in a hyperdopaminergic mouse model of bipolar disorder.

Authors:  Jordy van Enkhuizen; Mark A Geyer; Adam L Halberstadt; Xiaoxi Zhuang; Jared W Young
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8.  Neural Correlates of Impaired Reward-Effort Integration in Remitted Bulimia Nervosa.

Authors:  Stefanie Verena Mueller; Yosuke Morishima; Simon Schwab; Roland Wiest; Andrea Federspiel; Gregor Hasler
Journal:  Neuropsychopharmacology       Date:  2017-11-06       Impact factor: 7.853

9.  Reward learning in unmedicated women with bulimia nervosa: A pilot investigation.

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Journal:  J Psychiatr Res       Date:  2021-02-03       Impact factor: 4.791

10.  Pleasurable music affects reinforcement learning according to the listener.

Authors:  Benjamin P Gold; Michael J Frank; Brigitte Bogert; Elvira Brattico
Journal:  Front Psychol       Date:  2013-08-21
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