An immunohistochemical study of heat shock protein-27 in the hippocampus in a gerbil model of cerebral ischemia and ischemic tolerance.

Preconditioning of the gerbil brain with a 2-min period of sublethal ischemia protects against neuronal damage following a subsequent 3-min period of ischemia which normally damages CA1 neurons of the hippocampus (ischemic tolerance). In this study, we investigated the role of a small stress protein, heat shock protein-27, in the induction of ischemic tolerance. For this purpose, we used immunohistochemistry with an antibody against heat shock protein-27. Normal hippocampus contained very low levels of heat shock protein-27. The preconditioning ischemia for 2 min caused little changes in the heat shock protein-27 immunostaining in CA1 neurons but an increase in heat shock protein-27 immunostaining in a small number of astrocytes in the CA3 region and in many astrocytes in the dentate hilus. The second ischemia for 3 min caused no specific changes in heat shock protein-27 immunostaining in CA1 neurons both with and without tolerance in early reperfusion periods. After seven days, destruction of CA1 neurons occurred in animals without preconditioning and reactive astrocytes were intensely immunostained for heat shock protein-27. An intense heat shock protein-27 immunostaining was also seen in astrocytes in the dentate hilus after the second ischemia in both groups. Thus, we observed no temporal correlation between the induction of heat shock protein-27 and the manifestation of ischemic tolerance in the CA1 neurons. Most intense heat shock protein-27 immunostaining was observed in reactive astrocytes that accumulated in the damaged CA1 region and dentate hilus.(ABSTRACT TRUNCATED AT 250 WORDS)