Summary

Influx of Ca*+ through the NMDA subtype of glutamate receptor is widely accepted as a trigger for many forms of neural plasticity. However, direct support for this model has been elusive, since indirect activation of den-dritic voltage-sensitive Ca*+ channels is difficult to ex-clude. We have optically measured synaptically induced changes in cytoplasmic free Ca*+ concentration in pyra-midal cell dendrites in hippocampal slices. Steady post-synaptic depolarization to the synaptic reversal poten-tial eliminated the effect of voltage-sensitive Ca*+ channels. Under these conditions, synaptically induced Ca*+ transients were observed, which were blocked by the NMDA receptor antagonist APV. In addition, the magnitude of LTP was diminished when induced with the postsynaptic membrane held at progressively more positive potentials. LTP could be completely suppressed at potentials near +lOO mV. These results provide im-portant experimental support for a role for Ca*+ influx through NMDA receptors in synaptic plasticity