Microglia activation after neonatal hypoxic-ischemia.
The inflammatory response following hypoxic-ischemia (HI) in the neonate is largely unknown. Presently, the expression of microglial antigens and the beta-amyloid precursor protein (APP) were studied in relation to a dendrosomatic marker of neuronal injury (microtubule associated protein II; MAP II). HI was induced in 7-day-old rats by the combined unilateral carotid ligation and hypoxia. The pups (n = 23) were perfusion fixed 2-3 h, 24 h, 2-4 days and 14 days after HI and compared to sham-operated controls (n = 6). Antibodies were used for detection of the major histocompatibility complex II (OX-6), major histocompatibility complex I (OX-18) and complement receptor type 3 (OX-42), APP (APP 676-695) and MAP II (monoclonal MAP II) antigens. There was a transient APP expression 2-3 h after HI. A slight increase of microglial antigens (OX-18) was seen in the white matter 2 h after HI followed by a marked increase of OX-18, OX-6, OX-42 antigens 24 h-3-4 days in most injured regions with exception of the thalamus where a delayed (14 days) microglial response was seen. The latter event was parallelled by a delayed loss of MAP II. In conclusion, intense microglial expression occurs after neonatal HI either with an acute or delayed time-course depending on brain region.
McRae
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Department of Anatomy and Cell Biology, University of Göteborg, Sweden.
Gilland
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Bona
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Hagberg
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H
D016564:Amyloid beta-Protein Precursor / Q000276:immunology; D000818:Animals; D000906:Antibodies; D002540:Cerebral Cortex; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D007150:Immunohistochemistry; D007231:Infant, Newborn; D007511:Ischemia / Q000503:physiopathology*; D017628:Microglia / Q000378:metabolism*; D051381:Rats; D013788:Thalamus
D016564:Amyloid beta-Protein Precursor; D000906:Antibodies