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The translocation of synaptic Zn 2+  to the cytosolic compartment has been studied to understand Zn 2+  neurotoxicity in neurological diseases. However, it is unknown whether the moderate increase in Zn 2+  in the cytosolic compartment affects memory processing in the hippocampus. In the present study, the moderate increase in cytosolic Zn 2+  in the hippocampus was induced with clioquinol (CQ), a zinc ionophore. Zn 2+  delivery by Zn-CQ transiently attenuated CA1 long-term potentiation (LTP) in hippocampal slices prepared 2 h after i.p. injection of Zn-CQ into rats, when intracellular Zn 2+  levels was transiently increased in the CA1 pyramidal cell layer, followed by object recognition memory deficit. Object recognition memory was transiently impaired 30 min after injection of ZnCl 2  into the CA1, but not after injection into the dentate gyrus that did not significantly increase intracellular Zn 2+  in the granule cell layer of the dentate gyrus. Object recognition memory deficit may be linked to the preferential increase in Zn 2+  and/or the preferential vulnerability to Zn 2+  in CA1 pyramidal neurons. In the case of the cytosolic increase in endogenous Zn 2+  in the CA1 induced by 100 mM KCl, furthermore, object recognition memory was also transiently impaired, while ameliorated by co-injection of CaEDTA to block the increase in cytosolic Zn 2+ . The present study indicates that the transient increase in cytosolic Zn 2+  in CA1 pyramidal neurons reversibly impairs object recognition memory.

Transient Increase in Zn2+ in Hippocampal CA1 Pyramidal Neurons Causes Reversible Memory Deficit