Neuronal injury and expression of 72-kDa heat-shock protein after forebrain ischemia in the rat.

We evaluated the relationship between the induction of the 72-kDa heat-shock protein (hsp 72) and the presence of necrotic neurons in the rat hippocampus, 48 h after an 8-min episode of forebrain ischemia in eight rates. Hsp 72 was detected using the monoclonal antibody C92 on vibratome brain tissue sections. Hematoxylin and eosin (H&E) staining on adjacent paraffin-embedded sections was used to determine histopathological features. All morphologically intact CA1/2 neurons, 70% of which are destined to become necrotic 7 days after ischemia, exhibited intense hsp 72 staining, while necrotic or damaged neurons were devoid or low in hsp 72. Hsp 72 was also detected in CA3 neurons destined to survive 7 days after ischemia. Blood vessels positive for hsp 72 were detected in focal brain regions, in which severely damaged neurons were either devoid or low in hsp 72 staining. Occasional glial cells expressed hsp 72 in both normal and damaged brain regions. Hsp 72 response to a transient forebrain ischemia seemingly reflects differences in the selective ischemic vulnerability of CA1/2 and CA3 neurons. Further, the presence of hsp 72 within a neuron is likely only a marker of stress and is not necessarily indicative of eventual neuronal survival.