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

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  • Jan Józef Szczypiński
    Laboratory of Brain Imaging, Neurobiology Center , Nencki Institute of Experimental Biology, Polish Academy of Sciences , 3 Pasteur Street, 02-093 Warsaw , Poland
  • Mateusz Gola
    Swartz Center for Computational Neuroscience , Institute of Neural Computations , University of California San Diego , 9500 Gilman Drive, #0559 , La Jolla, CA 92093-0559 , USA

書誌事項

公開日
2018-03-24
DOI
  • 10.1515/revneuro-2017-0091
公開者
Walter de Gruyter GmbH

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<jats:title>Abstract</jats:title> <jats:p>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.</jats:p>

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