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Licensed Unlicensed Requires Authentication Published by De Gruyter March 24, 2018

Dopamine dysregulation hypothesis: the common basis for motivational anhedonia in major depressive disorder and schizophrenia?

  • Jan Józef Szczypiński ORCID logo EMAIL logo and Mateusz Gola


Abnormalities in reward processing are crucial symptoms of major depressive disorder (MDD) and schizophrenia (SCH). Recent neuroscientific findings regarding MDD have led to conclusions about two different symptoms related to reward processing: motivational and consummatory anhedonia, corresponding, respectively, to impaired motivation to obtain rewards (‘wanting’), and diminished satisfaction from consuming them (‘liking’). One can ask: which of these is common for MDD and SCH. In our review of the latest neuroscientific studies, we show that MDD and SCH do not share consummatory anhedonia, as SCH patients usually have unaltered liking. Therefore, we investigated whether motivational anhedonia is the common symptom across MDD and SCH. With regard to the similarities and differences between the neural mechanisms of MDD and SCH, here we expand the current knowledge of motivation deficits and present the common underlying mechanism of motivational anhedonia – the dopamine dysregulation hypothesis – stating that any prolonged dysregulation in tonic dopamine signaling that exceeds the given equilibrium can lead to striatal dysfunction and motivational anhedonia. The implications for further research and treatment of MDD and SCH are also discussed.


J. Szczypiński was supported by the Polish National Science Centre, OPUS grant (2016/21/B/HS6/01143). M. Gola was supported by the Polish Ministry of Science scholarships (1057/MOB/2013/0 and 469/STYP/10/2015), scholarship of The Kosciuszko Foundation, and Polish National Science Centre, OPUS grant (2014/15/B/HS6/03792).

  1. Conflict of interest statement: The authors report no conflicts of interest with respect to the content of this manuscript.


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Received: 2017-10-30
Accepted: 2018-01-30
Published Online: 2018-03-24
Published in Print: 2018-09-25

©2018 Walter de Gruyter GmbH, Berlin/Boston

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