Alterations in τ Immunostaining in the Rat Hippocampus Following Transient Cerebral Ischemia

• Published in: Journal of cerebral blood flow and metabolism 1994-07, Vol.14 (4), p.554-564
• Main Authors: Geddes, James W., Schwab, Claudia, Craddock, Susan, Wilson, Janice L., Pettigrew, L. Creed
• Format: Article
• Language: English
• Subjects: Animals; Benzoxazines; Biological and medical sciences; Coloring Agents; Heat-Shock Proteins - metabolism; Hippocampus - drug effects; Hippocampus - metabolism; Immunohistochemistry - methods; Ischemic Attack, Transient - metabolism; Kainic Acid - pharmacology; Male; Medical sciences; Microtubule-Associated Proteins - metabolism; Neurology; Oxazines; Rats; Rats, Wistar; Staining and Labeling; tau Proteins - metabolism; Vascular diseases and vascular malformations of the nervous system
• ISSN: 0271-678X; 1559-7016
• DOI: 10.1038/jcbfm.1994.69

Previous studies in gerbils have shown that cytoskeletal disruption and a loss of the dendritic microtubule-associated protein, MAP2, may occur after short periods of transient global ischemia. τ, a predominantly axonal microtubule-associated protein, has not been examined following ischemia. We compared neuronal damage with alterations in MAP2, τ, and 72-kD heat shock protein (HSP72) immunostaining at various reperfusion times following 20 min of ischemia in the rat four-vessel occlusion model. τ accumulated in neuronal cell bodies throughout the hippocampal formation 30 min to 2 h after the ischemic insult. Perikaryal τ 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 τ 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 τ immunostaining is not the direct result of excitotoxic insult, as intrahippocampal injection of kainic acid did not cause the somal accumulation of τ, but did cause disruption of MAP2 immunostaining. Taken together, the results suggest that the somal accumulation of τ is an early, sensitive, and selective marker of ischemic insult.