Amplitude fluctuations of

Abstract

Quantal analysis has provided evidence for a presynaptic contribution to long-term potentiation in hippocampal CA1 cells. This however leaves unexplained the observation that long-term potentiation has little or no effect on the NMDA receptor-mediated component of the synaptic signal. Here, I report that, in baseline conditions, the coefficient of variation of the AMPA/kainate receptor-mediated signal (CV A/K) is consistently larger than that of the NMDA component (CV NMDA), a result which can be explained if AMPA/kainate receptors are absent or nonfunctional at a proportion of synapses. Long-term potentiation is associated with a reduction in CV AK, but no change in either the average amplitude of the NMDA component or CV NMDA. This is consistent with the proposal that long-term potentiation induction uncovers clusters of latent AMPA/kainate receptors, with no change in transmitter release.