CYTOKINE TARGETS IN THE BRAIN: IMPACT ON NEUROTRANSMITTERS AND NEUROCIRCUITS: Review: Cytokine Targets in the Brain
Open accessAbstract
Increasing attention has been paid to the role of inflammation in a host of illnesses including neuropsychiatric disorders such as depression and anxiety. Activation of the inflammatory response leads to release of inflammatory cytokines and mobilization of immune cells both of which have been shown to access the brain and alter behavior. The mechanisms of the effects of inflammation on the brain have become an area of intensive study. Data indicate that cytokines and their signaling pathways including p38 mitogen-activated protein kinase have significant effects on the metabolism of multiple neurotransmitters such as serotonin, dopamine, and glutamate through impact on their synthesis, release, and reuptake. Cytokines also activate the kynurenine pathway, which not only depletes tryptophan, the primary amino acid precursor of serotonin, but also generates neuroactive metabolites that can significantly influence the regulation of dopamine and glutamate. Through their effects on neurotransmitter systems, cytokines impact neurocircuits in the brain including the basal ganglia and anterior cingulate cortex, leading to significant changes in motor activity and motivation as well as anxiety, arousal, and alarm. In the context of environmental challenge from the microbial world, these effects of inflammatory cytokines on the brain represent an orchestrated suite of behavioral and immune responses that subserve evolutionary priorities to shunt metabolic resources away from environmental exploration to fighting infection and wound healing, while also maintaining vigilance against attack, injury, and further pathogen exposure. Chronic activation of this innate behavioral and immune response may lead to depression and anxiety disorders in vulnerable individuals.
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Pro-inflammatory cytokines reduce the bioavailability of neurotransmitters critical for synaptic communication.
“Pro-inflammatory cytokines reduce the bioavailability of neurotransmitters critical for synaptic communication (61).”
From Chronic stress, neuroinflammation, and depression: an overview of pathophysiological mechanisms and emerging anti-inflammatories (2023) · cites this paper as [61]
Inflammation has been associated with antidepressant treatment non-responsiveness.
“inflammation has been associated with antidepressant treatment non-responsiveness9,32,35–37.”
From The role of inflammation in depression: from evolutionary imperative to modern treatment target (2016) · cites this paper as [35]
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“Pro-inflammatory cytokines cross the BBB or are produced by neuronal cells dysregulating neurotransmission and neurocircuitry (61).”
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Self-citation
- Authors
- Miller, A. H., Haroon, E., Raison, C. L., & Felger, J. C.
- Affiliations
- Emory University (US)
- University of Arizona (US)
- Corresponding author
- Miller, Andrew H.
- Venue
- Depression and Anxiety
- Publisher
- Wiley
- Published
- 2013-03-06
- Volume
- 30
- Issue
- 4
- Pages
- 297-306
- ISSN
- 1091-4269 (ISSN-L)
- PMC
- PMC4141874
- OpenAlex
- W1489805892
- Cited by
- 892
- References
- 105
- Citations by year
- 2026: 57 · 2025: 92 · 2024: 96 · 2023: 94 · 2022: 79 · 2021: 79 · 2020: 67 · 2019: 82 · 2018: 55 · 2017: 49 · 2016: 43 · 2015: 44 · 2014: 39 · 2013: 16
- FWCI
- 3.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Depression and Anxiety (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Abbott Laboratories
- Bristol-Myers Squibb
- Eli Lilly and Company
- Pfizer
- AstraZeneca
- GlaxoSmithKline
- F. Hoffmann-La Roche
- H. Lundbeck A/S
- National Institutes of Health (5u19mh069056-10, UL1TR000454)
- National Heart, Lung, and Blood Institute (R01HL073921)
- National Institute of Mental Health (U19-MH069056, R01MH083746, P50MH058922, R21 MH0771172, R01MH067990, F32MH093054, R03MH100273, R01MH087604, R01MH060723, K23MH091254, R01MH075102, K05MH069124)
- National Cancer Institute (P30CA138292)
- National Center for Research Resources (UL1RR025008)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- inflammatory cytokines, neuroinflammation, neurotransmitter metabolism, serotonin, dopamine, glutamate, kynurenine pathway, tryptophan depletion, p38 MAPK signaling, neural circuits, basal ganglia, anterior cingulate cortex, depression, anxiety, innate immune response, neuroimmune interactions
- MeSH terms
- Animals, Anxiety Disorders, Basal Ganglia, Blood-Brain Barrier, Depressive Disorder, Dopamine, Gyrus Cinguli, Humans, Inflammation, Serotonin, Signal Transduction, Cytokines
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