Abstract
Preconditioning the brain with sublethal ischemia induces tolerance to subsequent ischemie insult. Using [ 3H]quinuclidinyl benzilate (QNB), [ 3H]MK 801, [ 3H]cyclohexyladenosine, [ 3H]muscimol, and [ 3H]PN200-110, we investigated the alterations in neurotransmitter receptor and calcium channel binding in the gerbil hippocampus following ischemia with or without preconditioning. Two-minute forebrain ischemia, which produced no neuronal damage, resulted in no alterations in binding except for a slight reduction in [ 3H]QNB binding in the CA1 subfield. Three-minute ischemia destroyed the majority of CA1 pyramidal cells and caused, in CA1, reductions in binding of all ligands used. Preconditioning with 2-min ischemia followed by 4 days of reperfusion protected against CA1 neuronal damage and prevented the reductions in binding although [ 3H]QNB and [ 3H]PN200-110 binding transiently decreased in the early reperfusion period, suggesting downregulation. Thus, preconditioning protects against damage to the neurotransmission system as well as histopathological neuronal death.
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