The role of dopamine in inflammation-associated depression: mechanisms and therapeutic implications
Abstract
Studies investigating the impact of a variety of inflammatory stimuli on the brain and behavior have consistently reported evidence that inflammatory cytokines affect the basal ganglia and dopamine to mediate depressive symptoms related to motivation and motor activity. Findings have included inflammation-associated reductions in ventral striatal responses to hedonic reward, decreased dopamine and dopamine metabolites in cerebrospinal fluid, and decreased availability of striatal dopamine, all of which correlate with symptoms of anhedonia, fatigue, and psychomotor retardation. Similar relationships between alterations in dopamine-relevant corticostriatal reward circuitry and symptoms of anhedonia and psychomotor slowing have also been observed in patients with major depression who exhibit increased peripheral cytokines and other inflammatory markers, such as C-reactive protein. Of note, these inflammation-associated depressive symptoms are often difficult to treat in patients with medical illnesses or major depression. Furthermore, a wealth of literature suggests that inflammation can decrease dopamine synthesis, packaging, and release, thus sabotaging or circumventing the efficacy of standard antidepressant treatments. Herein, the mechanisms by which inflammation and cytokines affect dopamine neurotransmission are discussed, which may provide novel insights into treatment of inflammation-related behavioral symptoms that contribute to an inflammatory malaise.
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Inflammation can lead to changes in dopaminergic systems that are relevant to depression.
“Inflammation can also lead to changes in dopaminergic systems, with relevance for depression (See Felger, 2017 for review).”
From The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. (2018) · cites this paper as Felger, 2017
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Berk, M., Köhler‐Forsberg, O., Turner, M., Penninx, B. W. J. H., Wrobel, A., Firth, J., Loughman, A., Reavley, N. J., McGrath, J. J., Momen, N. C., et al. (2023) · World Psychiatry · doi:10.1002/wps.21110 · Cited by 336 · see citing works
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- Authors
- Felger, J. C.
- Affiliations
- Emory University (US)
- Corresponding author
- Felger, Jennifer C.
- ORCID
- Felger, Jennifer C.
- Venue
- Current Topics in Behavioral Neurosciences
- Publisher
- Springer International Publishing
- Published
- 2016
- Volume
- 31
- Pages
- 199-219
- ISSN
- 1866-3370 (ISSN-L)
- 1866-3389
- OpenAlex
- W2408044189
- Cited by
- 115
- References
- 146
- Citations by year
- 2026: 4 · 2025: 15 · 2024: 5 · 2023: 15 · 2022: 19 · 2021: 19 · 2020: 16 · 2019: 11 · 2018: 4 · 2017: 7
- FWCI
- 1.60
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Current topics in behavioral neurosciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- dopamine, cytokines, anhedonia, psychomotor retardation, ventral striatum, dopamine signaling, C-reactive protein, antidepressant resistance, fatigue, major depressive disorder, dopamine metabolites
- MeSH terms
- Animals, Depressive Disorder, Dopamine, Humans, Inflammation, Cytokines
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