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Excitotoxic brain damage in the rat induces interleukin-1beta protein in microglia and astrocytes: correlation with the progression of cell death.
Glia. 1999 Feb 15; 25(4):311-23.GLIA

Abstract

Interleukin-1 beta (IL-1beta) 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-1beta-mediated neurodegeneration. We have investigated the expression of IL-1beta protein by glial cells in vivo in response to NMDA receptor-mediated excitotoxicity in the rat parietal cortex and striatum. Expression of IL-1beta 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-1beta 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-1beta expression by microglia and astrocytes. However, IL-1beta-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-1beta expression. These studies reveal that IL-1beta is expressed specifically by microglia during the early response to excitotoxicity in the adult rat cortex and striatum. However, the widespread and delayed IL-1beta expression by astrocytes suggests diverse roles for IL-1beta in response to excitotoxicity.

Authors+Show Affiliations

School of Biological Sciences, University of Manchester, United Kingdom.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10028914

Citation

Pearson, V L., et al. "Excitotoxic Brain Damage in the Rat Induces Interleukin-1beta Protein in Microglia and Astrocytes: Correlation With the Progression of Cell Death." Glia, vol. 25, no. 4, 1999, pp. 311-23.
Pearson VL, Rothwell NJ, Toulmond S. Excitotoxic brain damage in the rat induces interleukin-1beta protein in microglia and astrocytes: correlation with the progression of cell death. Glia. 1999;25(4):311-23.
Pearson, V. L., Rothwell, N. J., & Toulmond, S. (1999). Excitotoxic brain damage in the rat induces interleukin-1beta protein in microglia and astrocytes: correlation with the progression of cell death. Glia, 25(4), 311-23.
Pearson VL, Rothwell NJ, Toulmond S. Excitotoxic Brain Damage in the Rat Induces Interleukin-1beta Protein in Microglia and Astrocytes: Correlation With the Progression of Cell Death. Glia. 1999 Feb 15;25(4):311-23. PubMed PMID: 10028914.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Excitotoxic brain damage in the rat induces interleukin-1beta protein in microglia and astrocytes: correlation with the progression of cell death. AU - Pearson,V L, AU - Rothwell,N J, AU - Toulmond,S, PY - 1999/2/24/pubmed PY - 1999/2/24/medline PY - 1999/2/24/entrez SP - 311 EP - 23 JF - Glia JO - Glia VL - 25 IS - 4 N2 - Interleukin-1 beta (IL-1beta) 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-1beta-mediated neurodegeneration. We have investigated the expression of IL-1beta protein by glial cells in vivo in response to NMDA receptor-mediated excitotoxicity in the rat parietal cortex and striatum. Expression of IL-1beta 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-1beta 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-1beta expression by microglia and astrocytes. However, IL-1beta-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-1beta expression. These studies reveal that IL-1beta is expressed specifically by microglia during the early response to excitotoxicity in the adult rat cortex and striatum. However, the widespread and delayed IL-1beta expression by astrocytes suggests diverse roles for IL-1beta in response to excitotoxicity. SN - 0894-1491 UR - https://www.unboundmedicine.com/medline/citation/10028914/Excitotoxic_brain_damage_in_the_rat_induces_interleukin_1beta_protein_in_microglia_and_astrocytes:_correlation_with_the_progression_of_cell_death_ DB - PRIME DP - Unbound Medicine ER -