PRESERVED NEUROTRANSMITTER RECEPTOR-BINDING FOLLOWING ISCHEMIA IN PRECONDITIONED GERBIL BRAIN

Preconditioning the brain with sublethal ischemia induces tolerance to subsequent ischemic insult. Using [H-3]quinuclidinyl benzilate (QNB), [H-3]MK 801, [H-3]cyclohexyladenosine, [H-3]muscimol, and [H-3]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 [H-3]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 [H-3]QNB and [H-3]PN200-110 binding transiently decreased in the early reperfusion period, suggesting down-regulation. Thus, preconditioning protects against damage to the neurotransmission system as well as histopathological neuronal death.