THE ROLE OF DENDRITIC ACTION-POTENTIALS AND CA2-TERM DEPRESSION IN HIPPOCAMPAL CA1 PYRAMIDAL NEURONS( INFLUX IN THE INDUCTION OF HOMOSYNAPTIC LONG)

Long-term depression (LTD) of synaptic efficacy at CA1 synapses is bel ieved to be a Ca2+-dependent process. We used high-speed fluorescence imaging and patch-clamp techniques to quantify the spatial distributio n of changes in intracellular Ca2+ accompanying the induction of LTD a t Schaffer collateral synapses in CA1 pyramidal neurons. Low-frequency stimulation (3 Hz), which was subthreshold for action potentials, pro duced small changes in [Ca2+](i) and failed to elicit LTD. Increasing the stimulus strength so that action potentials were generated produce d both robust LTD and increases in [Ca2+](i). Back-propagating action potentials at 3 Hz in the absence of synaptic stimulation also produce d increases in [Ca2+](i), but failed to induce LTD. When subthreshold synaptic stimulation was paired with back-propagating action potential s, however, large increases in [Ca2+](i) were observed and robust LTD was induced. The LTD was blocked by the N-methyl-D-aspartate receptor (NMDAr) antagonist APV, and stimulus-induced increases in [Ca2+](i) we re reduced throughout the neuron under these conditions. The LTD was a lso dependent on Ca2+ influx via voltage-gated Ca2+ channels (VGCCs), because LTD was severely attenuated or blocked by both nimodipine and Ni2+. These findings suggest that back-propagating action potentials c an exert a powerful control over the induction of LTD and that both VG CCs and NMDArs are involved in the induction of this form of plasticit y.