Microglia-astrocyte interactions after cortisone treatment in a neonatal hypoxia-ischemia model.
Microglial and astrocyte responses to glucocorticoid pretreatment in the neonate exposed to hypoxia-ischemia (HI) are largely unknown. The expression of microglial antigens and astrocytic proliferation was compared in neonatal rats exposed to HI with and without cortisone. HI was induced in 7 day old rats. One group of rats received cortisone within 24 h of birth. Immunocytochemical and immunoblot investigations were performed. Monoclonal antibodies (OX18 and OX42) were used for the detection of the major histocompatibility complex (MHC) class I antigens and complement receptor 3 (CR3) respectively. Antibodies directed against glial fibrillary acidic protein (GFAP) and microtubule associated protein II (MAP II) were used to evaluate the extent of brain damage. Cortisone treatment provoked a decline in the number of microglial cells but did not modify GFAP levels in control rats which were not exposed to HI. Neuronal damage was similar in control and cortisone treated rats exposed to HI. There were also similarities in the expression of CR3 antigens on microglia. However microglial cells expressing MHC class I antigens were less prevalent in rats exposed to HI only. Cortisone pretreatment enhanced the expression of MHC class I antigens. Astrocytic proliferation was intense in rats exposed to HI; however in rats treated with cortisone and exposed to HI there was a drastic reduction in astrocytic proliferation. In conclusion it is suggested that microglia which survive cortisone pretreatment become over-activated thereby preventing astrocytic proliferation.
McRae
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Institute of Anatomy and Cell Biology, University of Göteborg, Sweden.
Bona
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Hagberg
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D000818:Animals; D000831:Animals, Newborn; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000911:Antibodies, Monoclonal; D001253:Astrocytes / Q000737:chemistry / Q000166:cytology* / Q000502:physiology; D015153:Blotting, Western; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000098:blood supply / Q000473:pathology / Q000502:physiology; D002545:Brain Ischemia / Q000188:drug therapy / Q000503:physiopathology*; D002450:Cell Communication / Q000187:drug effects; D003348:Cortisone / Q000494:pharmacology*; D004195:Disease Models, Animal; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis / Q000276:immunology; D015395:Histocompatibility Antigens Class I / Q000032:analysis / Q000276:immunology; D002534:Hypoxia, Brain / Q000188:drug therapy / Q000503:physiopathology*; D007150:Immunohistochemistry; D008297:Male; D017628:Microglia / Q000737:chemistry / Q000166:cytology* / Q000502:physiology; D009336:Necrosis; D051381:Rats; D017208:Rats, Wistar; D015854:Up-Regulation / Q000502:physiology
D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D005904:Glial Fibrillary Acidic Protein; D015395:Histocompatibility Antigens Class I; D003348:Cortisone