Evidence map›Paper›PMID 37706039›Full record

ReviewFrontiers in psychiatry2023

Stress circuitry: mechanisms behind nervous and immune system communication that influence behavior.

Rose L Tong, Ubaidah N Kahn, Laura A Grafe, Frederick L Hitti, Nathan T Fried, Brian F Corbett

Abstract readReview
In one paragraph

Review in Frontiers in psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed.

  1. Antioxidant and Anti-Inflammatory Effects of InhaledPlants (Basel, Switzerland) · 2026
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  6. Anxiety disorders: a cross-sectional study of clinical and biological associations.Journal of neural transmission (Vienna, Austria : 1996) · 2026
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  16. The Role of Long Non-Coding RNA in Anxiety Disorders: A Literature Review.International journal of molecular sciences · 2025
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Rose L TongCorbett Laboratory, Department of Biology, Rutgers University, Camden, NJ, United States.
Ubaidah N KahnFried Laboratory, Department of Biology, Rutgers University, Camden, NJ, United States.
Laura A GrafeGrafe Laboratory, Department of Psychology, Bryn Mawr College, Bryn Mawr, PA, United States.
Frederick L HittiHitti Laboratory, Department of Neurological Surgery and Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, United States.
Nathan T FriedFried Laboratory, Department of Biology, Rutgers University, Camden, NJ, United States.
Brian F CorbettCorbett Laboratory, Department of Biology, Rutgers University, Camden, NJ, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory processes are increased by stress and contribute to the pathology of mood disorders. Stress is thought to primarily induce inflammation through peripheral and central noradrenergic neurotransmission. In healthy individuals, these pro-inflammatory effects are countered by glucocorticoid signaling, which is also activated by stress. In chronically stressed individuals, the anti-inflammatory effects of glucocorticoids are impaired, allowing pro-inflammatory effects to go unchecked. Mechanisms underlying this glucocorticoid resistance are well understood, but the precise circuits and molecular mechanisms by which stress increases inflammation are not as well known. In this narrative review, we summarize the mechanisms by which chronic stress increases inflammation and contributes to the onset and development of stress-related mood disorders. We focus on the neural substrates and molecular mechanisms, especially those regulated by noradrenergic signaling, that increase inflammatory processes in stressed individuals. We also discuss key knowledge gaps in our understanding of the communication between nervous and immune systems during stress and considerations for future therapeutic strategies. Here we highlight the mechanisms by which noradrenergic signaling contributes to inflammatory processes during stress and how this inflammation can contribute to the pathology of stress-related mood disorders. Understanding the mechanisms underlying crosstalk between the nervous and immune systems may lead to novel therapeutic strategies for mood disorders and/or provide important considerations for treating immune-related diseases in individuals suffering from stress-related disorders.

Indexed as

behaviorimmunityinflammationmoodnorepinephrinestress

Identifiers

PMID37706039
PMCPMC10495591

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.