Increase inω3 (peripheral type benzodiazepine) binding sites in the rat cortex and striatum after local injection of interleukin-1, tumour necrosis factor-α and lipopolysaccharide
Abstract
The possible involvement of lymphokines in the glial reaction/proliferation that follows brain injury has been investigated by measuring the density of omega 3 (peripheral type benzodiazepine) binding sites associated to glial cells and macrophages after local injection of lymphokines in the rat cerebral cortex and striatum. omega 3 Site densities were measured either by quantitative autoradiography in brain sections or by conventional binding in membrane using [3H]PK 14105 or [3H]PK 11195 as ligands. Intracortical or intrastriatal infusion of interleukin-1 (10 and 20 units) caused a marked increase in the density of omega 3 sites (+83% and +80%, respectively, when compared to saline-infused animals) around the injection site at 7 days postinjection. There was a good spatial correspondence between the autoradiographic distribution of omega 3 sites and the distribution of reactive astrocytes (as assessed by GFAP immunostaining) or acid phosphatase rich cells (phagocytes). Significant increases in omega 3 site densities were also observed in striatal homogenates 1 week after local administration of tumor necrosis factor-alpha (TNF-alpha). The maximal increase (+80%) was observed after the administration of 3 units, higher and lower doses resulting in smaller increases. Intrastriatal injection of E. coli lipopolysaccharide (LPS), a bacterial endotoxin known to stimulate interleukin-1 and TNF-alpha production by microglial cells in culture, also resulted in significant increases…
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Inflammatory cytokines such as interleukin-1β, tumour necrosis factor-α and interferon-γ have been shown to increase levels of TSPO in various cell types, including astrocytes.
“inflammatory cytokines such as interleukin-1β, tumour necrosis factor-α and interferon-γ have been shown to increase levels of TSPO in various cell types, including astrocytes [62–65]”
From Expression of the translocator protein of 18 kDa by microglia, macrophages and astrocytes based on immunohistochemical localization in abnormal human brain (2009) · cites this paper as [63]
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Self-citationMacGregor, D. G., & Stone, T. W. (1994) · Brain Research · doi:10.1016/0006-8993(94)91700-0 · Cited by 9 · see citing works
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- Authors
- Bourdiol, F., Toulmond, S., Serrano, A., Benavides, J., & Scatton, B.
- ORCID
- Scatton, B.
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 1991-03
- Volume
- 543
- Issue
- 2
- Pages
- 194-200
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W1980637734
- Cited by
- 77
- References
- 34
- Citations by year
- 2026: 1 · 2022: 1 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 1 · 2013: 1 · 2012: 2
- FWCI
- 4.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- translocator protein (TSPO), interleukin-1, TNF-α, lipopolysaccharide, glial activation, astrocytes, microglia, macrophages, cerebral cortex, striatum, brain injury, lymphokines, NMDA receptor, central benzodiazepine receptor, neuroinflammation
- MeSH terms
- Animals, Autoradiography, Cerebral Cortex, Corpus Striatum, Flumazenil, Humans, Interleukin-1, Lipopolysaccharides, Male, Membranes, N-Formylmethionine Leucyl-Phenylalanine, Rats, Inbred Strains, Receptors, GABA-A, Stereotaxic Techniques, Tumor Necrosis Factor-alpha, Rats, In Vitro Techniques
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