COMPLETE CEREBRAL-ISCHEMIA WITH SHORT-TERM SURVIVAL IN RAT INDUCED BYCARDIAC-ARREST .2. EXTRACELLULAR AND INTRACELLULAR ACCUMULATION OF APOLIPOPROTEIN-E AND APOLIPOPROTEIN-J IN THE BRAIN

The distribution of apolipoprotein E (ape E) and apolipoprotein J (ape J) was investigated immunocytochemically in rats at various time inte rvals after 10 min global cerebral ischemia (GCI) induced by cardiac a rrest. Strong apo E and weaker apo J immunoreactivity was found extrac ellularly in multiple deposits located close to the microvessels. Thes e deposits appeared 3 h after GCI and were present, but not in all the animals, at all time intervals studied post-GCI. In some rats, apo E immunoreactivity was also found in small necrotic foci. Widespread, ne uronal apo E immunostaining appeared 6 h post-GCI. However, the strong est neuronal apo E immunoreactivity was found 7 days post-GCI in those neurons, most often observed in the CA1 hippocampal region, exhibitin g signs of ischemic cell damage. These ischemically damaged neurons di splayed weaker immunoreactivity to apo J, despite its increase in the response to GCI in the various brain regions examined. Our data show t hat mechanisms operating in ischemia are able to supply large amounts of apo E and apo J to the brain tissue and suggest involvement of both apo E and apo J in a complex series of events occurring in the ischem ic brain. Perivascular deposits of apo E/apo J colocalized with amyloi d beta protein precursor epitopes that have been disclosed by us previ ously in this model. Whether this phenomenon is limited to postischemi c brain tissue, or can be encountered also in other pathological condi tions will require further elaboration.