Literature DB >> 29573379

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

Jan Józef Szczypiński1,2,3, Mateusz Gola4,5.   

Abstract

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.

Entities:  

Keywords:  dopamine; major depressive disorder; motivational anhedonia; reward system; schizophrenia

Mesh:

Substances:

Year:  2018        PMID: 29573379     DOI: 10.1515/revneuro-2017-0091

Source DB:  PubMed          Journal:  Rev Neurosci        ISSN: 0334-1763            Impact factor:   4.353


  12 in total

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Review 6.  Discovering the Lost Reward: Critical Locations for Endocannabinoid Modulation of the Cortico-Striatal Loop That Are Implicated in Major Depression.

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Review 9.  Ventral Striatal Reactivity in Compulsive Sexual Behaviors.

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10.  Loss of habenular Prkar2a reduces hedonic eating and increases exercise motivation.

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Journal:  JCI Insight       Date:  2020-12-03
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