ALTERATIONS IN TAU IMMUNOSTAINING IN THE RAT HIPPOCAMPUS FOLLOWING TRANSIENT CEREBRAL-ISCHEMIA

Previous studies in gerbils have shown that cytoskeletal disruption an d a loss of the dendritic microtubule-associated protein, MAP2, may oc cur after short periods of transient global ischemia. tau, a predomina ntly axonal microtubule-associated protein, has not been examined foll owing ischemia. We compared neuronal damage with alterations in MAP2, tau, and 72-kD heat shock protein (HSP72) immunostaining at various re perfusion times following 20 min of ischemia in the rat four-vessel oc clusion model. tau accumulated in neuronal cell bodies throughout the hippocampal formation 30 min to 2 h after the ischemic insult. Perikar yal tau immunostaining was transient in most regions, but persisted in polymorphic hilar neurons. This was accompanied by a loss of immunost aining in the target of many hilar neurons, the inner molecular layer of the dentate gyrus. The same neuronal populations that exhibited inc reased tau immunostaining of perikarya later displayed an induction of HSP72 immunoreactivity. In contrast, loss of MAP2 immunostaining was not consistently observed before neuronal death and did not correspond to HSP72 induction. The altered tau immunostaining is not the direct result of excitotoxic insult, as intrahippocampal injection of kainic acid did not cause the somal accumulation of tau, but did cause disrup tion of MAP2 immunostaining. Taken together, the results suggest that the somal accumulation of tau is an early, sensitive, and selective ma rker of ischemic insult.