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The role of zinc (Zn 2+ ), a modulator of N-methyl-D-aspartate (NMDA) receptors, in regulating long-term synaptic plasticity at hippocampal CA1 synapses is poorly understood. The effects of exogenous application of Zn 2+  and of chelation of endogenous Zn 2+  were examined on long-term potentiation (LTP) of stimulus-evoked synaptic transmission at Schaffer collateral (SCH) synapses in field CA1 of mouse hippocampal slices using whole-cell patch clamp and field recordings. Low micromolar concentrations of exogenous Zn 2+  enhanced the induction of LTP, and this effect required activation of NMDA receptors containing NR2B subunits. Zn 2+  elicited a selective increase in NMDA/NR2B fEPSPs, and removal of endogenous Zn 2+  with high-affinity Zn 2+  chelators robustly reduced the magnitude of stimulus-evoked LTP. Taken together, our data show that Zn 2+  at physiological concentrations enhances activation of NMDA receptors containing NR2B subunits, and that this effect enhances the magnitude of LTP.

Zinc enhances hippocampal long-term potentiation at CA1 synapses through NR2B containing NMDA receptors