The DOI matches its Crossref record; 109 of the 110 references it cites were found in a registry or an index.
Peripheral and central effects of repeated social defeat stress: Monocyte trafficking, microglial activation, and anxiety
Open accessAbstract
The development and exacerbation of depression and anxiety are associated with exposure to repeated psychosocial stress. Stress is known to affect the bidirectional communication between the nervous and immune systems leading to elevated levels of stress mediators including glucocorticoids (GCs) and catecholamines and increased trafficking of proinflammatory immune cells. Animal models, like the repeated social defeat (RSD) paradigm, were developed to explore this connection between stress and affective disorders. RSD induces activation of the sympathetic nervous system (SNS) and hypothalamic-pituitary-adrenal (HPA) axis activation, increases bone marrow production and egress of primed, GC-insensitive monocytes, and stimulates the trafficking of these cells to tissues including the spleen, lung, and brain. Recently, the observation that these monocytes have the ability to traffic to the brain perivascular spaces and parenchyma have provided mechanisms by which these peripheral cells may contribute to the prolonged anxiety-like behavior associated with RSD. The data that have been amassed from the RSD paradigm and others recapitulate many of the behavioral and immunological phenotypes associated with human anxiety disorders and may serve to elucidate potential avenues of treatment for these disorders. Here, we will discuss novel and key data that will present an overview of the neuroendocrine, immunological and behavioral responses to social stressors.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“Furthermore, chronic psychosocial stress promotes an increase in glucocorticoid (GC)-insensitive monocyte populations. Recent studies have also observed that these monocytes possess the ability to transmigrate across the blood–brain barrier, potentially contributing to the development of long-term anxiety-related behaviors [23].”
From Comparative Analysis of HPA-Axis Dysregulation and Dynamic Molecular Mechanisms in Acute Versus Chronic Social Defeat Stress (2025) · cites this paper as [23]
In the citing paper
“In addition, the physiological consequences of exposure to RSD are robustly associated with structural changes (e.g., atrophy, connectivity) to neural systems that modulate threat-sensitivity and anxiety-like behaviors (Reader et al., 2015).”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Reader et al., 2015
In the citing paper
“Repeated social defeat (RSD) is an ethologically relevant social stressor that recapitulates many of the stress-induced immune and behavioral outcomes of stress (Reader et al, 2015).”
From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Reader et al, 2015
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Diagnostic and Statistical Manual of Mental Disorders
Williams, J. B. W., & First, M. B. (2013) · Oxford University Press eBooks · doi:10.1093/acrefore/9780199975839.013.104 · Cited by 109,845
LeDoux, J. E. (2000) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.23.1.155 · Cited by 8,444
From inflammation to sickness and depression: when the immune system subjugates the brain
Dantzer, R., O'Connor, J. C., Freund, G. G., Johnson, R. W., & Kelley, K. W. (2008) · Nature Reviews Neuroscience · doi:10.1038/nrn2297 · Cited by 7,395 · cited 2×
“The mechanistic association between inflammation and depression is particularly well-established (Raison et al., 2006; Dantzer et al., 2008; Miller et al., 2009; Norman et al., 2010; Capuron and Miller, 2011), while the case continues to build for the mechanistic association between inflammation…”
BackgroundInflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression
Miller, A. H., Maletic, V., & Raison, C. L. (2009) · Biological Psychiatry · doi:10.1016/j.biopsych.2008.11.029 · Cited by 3,848 · cited 15×
“The mechanistic association between inflammation and depression is particularly well-established (Raison et al., 2006; Dantzer et al., 2008; Miller et al., 2009; Norman et al., 2010; Capuron and Miller, 2011), while the case continues to build for the mechanistic association between inflammation…”
BackgroundInfluentialFate Mapping Reveals Origins and Dynamics of Monocytes and Tissue Macrophages under Homeostasis
Yona, S., Kim, K.-W., Wolf, Y., Mildner, A., Varol, D., Breker, M., Strauss-Ayali, D., Viukov, S., Guilliams, M., Misharin, A., et al. (2013) · Immunity · doi:10.1016/j.immuni.2012.12.001 · Cited by 3,245 · cited 7×
“Moreover, data suggest that RSD-induced microglial activation is likely an upstream event of monocyte trafficking to the brain and this is dependent on receptors such as CCR2 and CX3CR1 in that increased microglia cytokine expression was still observed in CCR2KO and CX3CR1 KO mice that lacked both perivascular and par…”
BackgroundInfluentialCytokines sing the blues: inflammation and the pathogenesis of depression
Raison, C. L., Capuron, L., & Miller, A. H. (2006) · Trends in Immunology · doi:10.1016/j.it.2005.11.006 · Cited by 3,009 · cited 4×
“…are not fully understood, the individual response to prolonged or severe stressors contributes to the development and exacerbation of depression and anxiety (Maes et al., 1998; Kalynchuk et al., 2004; Raison et al., 2006; Norman et al., 2010; Capuron and Miller, 2011; Gilman et al., 2013).”
BackgroundInfluentialThe blood-brain barrier/neurovascular unit in health and disease
Hawkins, B. T., & Davis, T. P. (2005) · Pharmacological Reviews · doi:10.1124/pr.57.2.4 · Cited by 2,661 · cited 1×
“This idea that neuronal activity locally influences brain vasculature is reminiscent of the concept of a neurovascular unit (Hawkins and Davis, 2005).”
BackgroundJung, S., Aliberti, J., Graemmel, P., Sunshine, M. J., Kreutzberg, G. W., Sher, A., & Littman, D. R. (2000) · Molecular and Cellular Biology · doi:10.1128/mcb.20.11.4106-4114.2000 · Cited by 2,632 · cited 2×
“, 2011), while the fractalkine receptor is highly expressed by microglia (Jung et al., 2000).”
BackgroundIdentification of a unique TGF-β–dependent molecular and functional signature in microglia
Butovsky, O., Jedrychowski, M. P., Moore, C. S., Cialic, R., Lanser, A. J., Gabriely, G., Koeglsperger, T., Dake, B., Wu, P. M., Doykan, C. E., et al. (2014) · Nature Neuroscience · doi:10.1038/nn.3599 · Cited by 2,543 · cited 1×
“Because the brain is highly sensitive to increases in proinflammatory cytokines, microglia tend to be highly regulated by anti-inflammatory ligands and receptors (e.g., CD200/CD200R (Lyons et al., 2007), CX3CR1/CX3CL1 (Cardona et al., 2006), or TGFb/TGFbR (Butovsky et al., 2014)).”
BackgroundIdentification of splenic reservoir monocytes and their deployment to inflammatory sites
Swirski, F. K., Nahrendorf, M., Etzrodt, M., Wildgruber, M., Cortez-Retamozo, V., Panizzi, P., Figueiredo, J.-L., Kohler, R. H., Chudnovskiy, A., Waterman, P., et al. (2009) · Science · doi:10.1126/science.1175202 · Cited by 2,221 · cited 1×
“The idea that the spleen serves as an alternative source of monocyte trafficking is seen in several studies involving inflammatory challenges including myocardial infarction (Swirski et al., 2009) and stroke (Seifert et al., 2012).”
Background
Cited by
Sorted by citations
Microglia in physiology and disease
Wolf, S. A., Boddeke, H. W. G. M., & Kettenmann, H. (2017) · Annual Review of Physiology · doi:10.1146/annurev-physiol-022516-034406 · Cited by 1,426
Neuroimmune mechanisms of depression
Hodes, G. E., Kana, V., Menard, C., Merad, M., & Russo, S. J. (2015) · Nature Neuroscience · doi:10.1038/nn.4113 · Cited by 585
Pathogenesis of depression: Insights from human and rodent studies
Ménard, C., Hodes, G. E., & Russo, S. J. (2016) · Neuroscience · doi:10.1016/j.neuroscience.2015.05.053 · Cited by 593
“…of monocytes originating from the periphery in the brain (Wohleb et al., 2013), suggesting that blood brain-barrier (BBB) permeability may be affected by stress and could contribute to the establishment of depressive-like behaviors and mood disorders (Wohleb et al., 2014b, Reader et al., 2015).”
BackgroundAnimal models of major depression: drawbacks and challenges
Planchez, B., Surget, A., & Belzung, C. (2019) · Journal of Neural Transmission · doi:10.1007/s00702-019-02084-y · Cited by 480
Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal
Weber, M. D., Godbout, J. P., & Sheridan, J. F. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2016.102 · Cited by 283
“Repeated social defeat (RSD) is an ethologically relevant social stressor that recapitulates many of the stress-induced immune and behavioral outcomes of stress (Reader et al, 2015).”
BackgroundSelf-citation
Metadata
- Authors
- Reader, B. F., Jarrett, B. L., McKim, D. B., Wohleb, E. S., Godbout, J. P., & Sheridan, J. F.
- Affiliations
- The Ohio State University Wexner Medical Center (US)
- Yale University (US)
- Corresponding author
- Sheridan, J.F.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2015-03
- Volume
- 289
- Pages
- 429-442
- ISSN
- 0306-4522 (ISSN-L)
- PMC
- PMC4536813
- OpenAlex
- W2024776501
- Cited by
- 179
- References
- 110
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 13 · 2023: 12 · 2022: 18 · 2021: 20 · 2020: 9 · 2019: 19 · 2018: 20 · 2017: 20 · 2016: 20 · 2015: 12
- FWCI
- 1.92
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (R01-MH-093473, R01-MH093472)
- NIH/NIDCR (T32-DE014320)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- repeated social defeat stress, anxiety-like behavior, monocyte trafficking, microglial activation, neuroimmune interactions, hypothalamic-pituitary-adrenal axis, sympathetic nervous system, depression, psychosocial stress
- MeSH terms
- Animals, Anxiety, Dominance-Subordination, Humans, Monocytes, Stress, Psychological, Microglia
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review