EFFECT OF 2,6-DIISOPROPYLPHENOL ON THE DELAYED HIPPOCAMPAL CELL LOSS FOLLOWING TRANSIENT FOREBRAIN ISCHEMIA IN THE GERBIL

We examined the protective activity of 2,6-diisopropylphenol on mortal ity and delayed hippocampal cell death induced by transient cerebral i schemia In the gerbil. Forebrain ischemia was produced by bilaterally occludlng the common carotid arteries for 10 minutes; then the blood s upply to the brain was restored. The number of survivors was counted f or 8 days, and the histopathological damage in the CA1 region of the h ippocampus was scored according to the semiquantitative scale of Rudol phi and Colleagues. When intraperitoneally injected immediately after the ischemic attack, 2,6-diisopropylphenol (25, 50, 100 mg kg(-1)) pro duced no significant reduction in the rate of mortality in comparison with its vehicle. However, the survivors that had received the compoun d at the dose of 50 and 100 mg kg(-1) elicited a significant increase in the number of viable pyramidal cells in the CA1 hippocampal region. Moreover, we obtained similar results by injecting the compound 30 mi nutes after the release of the carotid artery occlusion. These results suggest that 2,6-diisopropylphenol, although it does not show any cap ability of improving the rate of survival, it elicits protective prope rties against the transient forebrain ischemia-induced delayed hippoca mpal neuronal death.