Jw. Geddes et al., ALTERATIONS IN TAU IMMUNOSTAINING IN THE RAT HIPPOCAMPUS FOLLOWING TRANSIENT CEREBRAL-ISCHEMIA, Journal of cerebral blood flow and metabolism, 14(4), 1994, pp. 554-564
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.