Alterations in tau immunostaining in the XXXX hippocampus following transient cerebral ischemia.

@entity63 @entity34445 @entity19514 @entity4176 @entity35 @entity19744 @entity528
Previous studies in gerbils have shown that cytoskeletal disruption and a loss of the dendritic microtubule-associated protein, @entity19744 , may occur after short periods of transient global @entity63 . tau, a predominantly axonal microtubule-associated protein, has not been examined following @entity63 . We compared neuronal damage with alterations in @entity19744 , tau, and 72-kD @entity19514 ( @entity34445 ) immunostaining at various reperfusion times following 20 min of @entity63 in the @entity35 four-vessel occlusion model. tau accumulated in neuronal cell bodies throughout the hippocampal formation 30 min to 2 h after the @entity63 insult. Perikaryal tau immunostaining was transient in most regions, but persisted in polymorphic hilar neurons. This was accompanied by a loss of immunostaining in the target of many hilar neurons, the inner molecular layer of the dentate gyrus. The same neuronal populations that exhibited increased tau immunostaining of perikarya later displayed an induction of @entity34445 immunoreactivity. In contrast, loss of @entity19744 immunostaining was not consistently observed before @entity528 and did not correspond to @entity34445 induction. The altered tau immunostaining is not the direct result of excitotoxic insult, as intrahippocampal injection of @entity4176 did not cause the somal accumulation of tau, but did cause disruption of @entity19744 immunostaining. Taken together, the results suggest that the somal accumulation of tau is an early, sensitive, and selective marker of @entity63 insult.
