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Is depression associated with dysfunction of the central reward system?


Martin-Soelch, C (2009). Is depression associated with dysfunction of the central reward system? Biochemical Society Transactions, 37(Pt 1):313-317.

Abstract

The neural substrates of MDD (major depressive disorder) are complex and not yet fully understood. In the present review, I provide a short overview of the findings supporting the hypothesis of a dysfunctional dopamine system in the pathophysiology of depression. Because the mesocorticolimbic dopamine system is involved in reward processing, it has been hypothesized that a reduced function of this system could underlie the anhedonia and amotivation associated with depression. This hypothesis is supported by several observations providing indirect evidence for reduced central dopaminergic transmission in depression. However, some of the differences observed between controls and depressed patients in dopamine function seem to be specific to a subsample of patients, and influenced by the methods chosen. Studies that investigated the neural bases of some MDD behavioural symptoms showed that anhedonia, loss of motivation and the diminished ability to concentrate or make decisions could be associated with a blunted reaction to positive reinforcers and rewards on one side, and with a bias towards negative feedback on the other side. Only a few studies have investigated the neural basis of anhedonia and the responses to rewards in MDD subjects, mostly evidencing a blunted response to reward signals that was associated with reduced brain activation in regions associated with the brain reward system. In conclusion, there is evidence for a dysfunction of the dopamine system in depression and for blunted response to reward signals. However, the exact nature of this dysfunction is not yet clear and needs to be investigated in further studies.

The neural substrates of MDD (major depressive disorder) are complex and not yet fully understood. In the present review, I provide a short overview of the findings supporting the hypothesis of a dysfunctional dopamine system in the pathophysiology of depression. Because the mesocorticolimbic dopamine system is involved in reward processing, it has been hypothesized that a reduced function of this system could underlie the anhedonia and amotivation associated with depression. This hypothesis is supported by several observations providing indirect evidence for reduced central dopaminergic transmission in depression. However, some of the differences observed between controls and depressed patients in dopamine function seem to be specific to a subsample of patients, and influenced by the methods chosen. Studies that investigated the neural bases of some MDD behavioural symptoms showed that anhedonia, loss of motivation and the diminished ability to concentrate or make decisions could be associated with a blunted reaction to positive reinforcers and rewards on one side, and with a bias towards negative feedback on the other side. Only a few studies have investigated the neural basis of anhedonia and the responses to rewards in MDD subjects, mostly evidencing a blunted response to reward signals that was associated with reduced brain activation in regions associated with the brain reward system. In conclusion, there is evidence for a dysfunction of the dopamine system in depression and for blunted response to reward signals. However, the exact nature of this dysfunction is not yet clear and needs to be investigated in further studies.

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Additional indexing

Item Type:Journal Article, not refereed, further contribution
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Psychiatry and Psychotherapy
Dewey Decimal Classification:610 Medicine & health
Date:2009
Deposited On:03 Jun 2009 06:47
Last Modified:05 Apr 2016 13:14
Publisher:Portland Press
ISSN:0300-5127
Additional Information:The Version of Record (VoR) is available at www.biochemj.org
Publisher DOI:10.1042/BST0370313
PubMed ID:19143654
Permanent URL: http://doi.org/10.5167/uzh-18698

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