MICROGLIA ACTIVATION AFTER NEONATAL HYPOXIC-ISCHEMIA

The inflammatory response following hypoxic-ischemia (HI) in the neona te is largely unknown. Presently, the expression of microglial antigen s and the beta-amyloid precursor protein (APP) were studied in relatio n 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 perfu sion 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 histocompatibili ty complex I(OX-18) and complement receptor type 3 (OX-42), APP (APP 6 76-695) and MAP II (monoclonal MAP II) antigens. There was a transient APP expression 2-3 h after HI. A slight increase of microglial antige ns (OX-18) was seen in the white matter 2 h after HI followed by a mar ked increase of OX-18, OX-6, OX-42 antigens 24 h-3-4 days in most inju red regions with exception of the thalamus where a delayed (14 days) m icroglial response was seen. The latter event was parallelled by a del ayed loss of MAP II. In conclusion, intense microglial expression occu rs after neonatal HI either with an acute or delayed time-course depen ding on brain region.