A neuromodulatory role of interleukin-1β in the hippocampus
Open accessAbstract
It is widely accepted that interleukin-1beta (IL-1beta), a cytokine produced not only by immune cells but also by glial cells and certain neurons influences brain functions during infectious and inflammatory processes. It is still unclear, however, whether IL-1 production is triggered under nonpathological conditions during activation of a discrete neuronal population and whether this production has functional implications. Here, we show in vivo and in vitro that IL-1beta gene expression is substantially increased during long-term potentiation of synaptic transmission, a process considered to underlie certain forms of learning and memory. The increase in gene expression was long lasting, specific to potentiation, and could be prevented by blockade of potentiation with the N-methyl-D-aspartate (NMDA) receptor antagonist, (+/-)-2-amino-5-phosphonopentanoic acid (AP-5). Furthermore, blockade of IL-1 receptors by the specific interleukin-1 receptor antagonist (IL-1ra) resulted in a reversible impairment of long-term potentiation maintenance without affecting its induction. These results show for the first time that the production of biologically significant amounts of IL-1beta in the brain can be induced by a sustained increase in the activity of a discrete population of neurons and suggest a physiological involvement of this cytokine in synaptic plasticity.
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Expression of IL-1β increases during long-term potentiation in neurons.
“In 1998, Schneider H. et al. could show that expression of IL-1β increases during long-term potentiation in neurons, which consists in a synaptic strengthening process implicated in learning and memory (203).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [203]
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- Authors
- Schneider, H., Pitossi, F., Balschun, D., Wagner, A., del Rey, A., & Besedovsky, H. O.
- Affiliations
- Philipps University of Marburg (DE)
- Institute of Physiology, Division of Immunophysiology, Philipps University Marburg, Deutschhausstrasse 2, 35037 Marburg, Germany; and Institute for Neurobiology, Department of Neurophysiology, P.O. Box 1860, 39008 Magdeburg, Germany
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1998-06-23
- Volume
- 95
- Issue
- 13
- Pages
- 7778-7783
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC22755
- OpenAlex
- W1970891635
- Cited by
- 498
- References
- 51
- Citations by year
- 2026: 6 · 2025: 13 · 2024: 13 · 2023: 6 · 2022: 20 · 2021: 26 · 2020: 23 · 2019: 18 · 2018: 26 · 2017: 24 · 2016: 20 · 2015: 20 · 2014: 30 · 2013: 19 · 2012: 25
- FWCI
- 8.27
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- IL-1β, hippocampus, long-term potentiation, synaptic plasticity, interleukin-1 receptor antagonist, NMDA receptor, AP5, learning and memory, neuroinflammation, cytokine gene expression, synaptic transmission
- MeSH terms
- Animals, Gene Expression Regulation, Hippocampus, Interleukin-1, Male, Movement, Neuronal Plasticity, Recombinant Proteins, Sialoglycoproteins, Rats, Wistar, Receptors, Interleukin-1, Long-Term Potentiation, Rats, Interleukin 1 Receptor Antagonist Protein
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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