Excitotoxic brain damage in the rat induces interleukin-1β protein in microglia and astrocytes: Correlation with the progression of cell death
✍ Scribed by Victoria Louise Pearson; Nancy Jane Rothwell; Sylvie Toulmond
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 552 KB
- Volume
- 25
- Category
- Article
- ISSN
- 0894-1491
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✦ Synopsis
Interleukin-1 beta (IL-1) has been proposed as a mediator of several forms of brain damage, including that induced by excitotoxins. In vitro studies suggest that glial cells are the effector cells of IL-1-mediated neurodegeneration. We have investigated the expression of IL-1 protein by glial cells in vivo in response to NMDA receptor-mediated excitotoxicity in the rat parietal cortex and striatum.
Expression of IL-1 by glial cells was investigated using immunocytochemistry 30 min to 7 days after infusion of the NMDA agonist cis-2,4-methanoglutamate (MGlu; 10 nmol) into the cortex. Early expression (1-4 h) of IL-1 by microglia was directly related to lesion development. Later expression by microglia (up to 24 h), and by astrocytes (2-7 days), was widespread compared to the area involved in excitotoxic cell death and co-localised with areas of reactive gliosis.
Infusion of MGlu into the striatum induced a similar temporal pattern of IL-1 expression by microglia and astrocytes. However, IL-1-expressing glial cells were localised strictly to the area of striatal cell death. Infusion of PBS or a subtoxic dose of MGlu into the cortex or striatum induced only limited neuronal death and negligible glial IL-1 expression.
These studies reveal that IL-1 is expressed specifically by microglia during the early response to excitotoxicity in the adult rat cortex and striatum. However, the widespread and delayed IL-1 expression by astrocytes suggests diverse roles for IL-1 in response to excitotoxicity.