The stress-induced cytokine interleukin-6 decreases the inhibition/excitation ratio in the rat temporal cortex via trans-signaling
Open accessAbstract
Background Although it is known that stress elevates the levels of pro-inflammatory cytokines and promotes hyper-excitable central conditions, a causal relationship between these two factors has not yet been identified. Recent studies suggest that increases in interleukin 6 (IL-6) levels are specifically associated with stress. We hypothesized that IL-6 acutely and directly induces cortical hyper-excitability by altering the balance between synaptic excitation and inhibition.Methods We used patch-clamp to determine the effects of exogenous or endogenous IL-6 on electrically evoked postsynaptic currents on a cortical rat slice preparation. We used control subjects or animals systemically injected with lipopolysaccharide or subjected to electrical foot-shock as rat models of stress.Results In control animals, IL-6 did not affect excitatory postsynaptic currents but selectively and reversibly reduced the amplitude of inhibitory postsynaptic currents with a postsynaptic effect. The IL-6-induced inhibitory postsynaptic currents decrease was inhibited by drugs interfering with receptor trafficking and/or internalization, including wortmannin, Brefeldin A, 2-Br-hexadecanoic acid, or dynamin peptide inhibitor. In both animal models, stress-induced decrease in synaptic inhibition/excitation ratio was prevented by prior intra-ventricular injection of an analog of the endogenous IL-6 trans-signaling blocker gp130.Conclusions Our results suggest that stress-induced IL-6 shifts the balance between synaptic inhibition and excitation in favor of the latter, possibly by decreasing the density of functional γ-aminobutyric acid A receptors, accelerating their removal and/or decreasing their insertion rate from/to the plasma membrane. We speculate that this mechanism could contribute to stress-induced detrimental long-term increases in central excitability present in a variety of neurological and psychiatric conditions.
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Administration of IL-6 to cortical rat slice preparations decreased GABAergic inhibition shifting the balance to glutamatergic central hyperexcitability.
“Garcia-Oscos and colleagues found that administration of IL-6 to cortical rat slice preparations decreased GABAergic inhibition shifting the balance to glutamatergic central hyperexcitability (143).”
From Chronic stress, neuroinflammation, and depression: an overview of pathophysiological mechanisms and emerging anti-inflammatories (2023) · cites this paper as [143]
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“Garcia-Oscos and colleagues found that administration of IL-6 to cortical rat slice preparations decreased GABAergic inhibition shifting the balance to glutamatergic central hyperexcitability (143).”
BackgroundThe role of interleukin-6 signaling in nervous tissue
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- Authors
- Garcia-Oscos, F., Salgado, H., Hall, S., Thomas, F., Farmer, G. E., Bermeo, J., Galindo, L. C., Ramirez, R. D., D'Mello, S., Rose-John, S., & Atzori, M.
- Affiliations
- The University of Texas at Dallas (US)
- Universidad Nacional Autónoma de México (MX)
- Corresponding author
- Atzori, Marco
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2012-04
- Volume
- 71
- Issue
- 7
- Pages
- 574-582
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC4732871
- OpenAlex
- W2083811331
- Cited by
- 105
- References
- 81
- Citations by year
- 2026: 10 · 2025: 11 · 2024: 7 · 2023: 12 · 2022: 7 · 2021: 8 · 2020: 5 · 2019: 3 · 2018: 6 · 2017: 6 · 2016: 6 · 2015: 9 · 2014: 7 · 2013: 3 · 2012: 5
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Deutsche Forschungsgemeinschaft (SFB654, SFB841, SFB877)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- interleukin-6, stress, trans-signaling, gp130, inhibitory postsynaptic currents, excitatory postsynaptic currents, GABAA receptor, receptor trafficking, receptor internalization, lipopolysaccharide, footshock, temporal cortex, inflammatory cytokines, central hyperexcitability
- MeSH terms
- Wortmannin, Interleukin-6 Inhibitors, Androstadienes, Animals, Disease Models, Animal, Drug Interactions, Electric Stimulation, Lipopolysaccharides, Muscimol, Oligopeptides, Palmitates, Stress, Psychological, Temporal Lobe, Interleukin-6, Excitatory Postsynaptic Potentials, Brefeldin A, Cytokine Receptor gp130, Rats, Inhibitory Postsynaptic Potentials
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 ›
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