Dependence of calcium influx in neocortical cells on temporal structure of depolarization, number of spikes, and blockade of NMDA receptors

Increase of intracellular [Ca 2+ ] evoked by action potentials in a cell can induce long‐term synaptic plasticity even without concomitant presynaptic stimulation. We used optical recording of the fluorescence of a Ca 2+ ‐indicator Oregon Green to investigate whether differences in results obtained with modifications of that purely postsynaptic induction protocol could be due to differential Ca 2+ influx. We compared changes of the somatic [Ca 2+ ] in layer II–III pyramidal cells in slices of rat visual cortex evoked by bursts of depolarization pulses and long depolarizing steps. During weak depolarizations, the Ca 2+ influx was proportional to the amplitude and duration of the depolarization. With suprathreshold depolarizations, the Ca 2+ influx was proportional to the number of action potentials. Because the burst depolarizations evoked more spikes than did the long duration steps, this burst protocol led to a larger Ca 2+ influx. With all stimulation protocols, the spike‐induced Ca 2+ influx was reduced during blockade of N ‐methyl‐ D ‐aspartate (NMDA) receptors. Differences in intracellular [Ca 2+ ] increases thus may be one reason for differential effects of purely postsynaptic challenges on synaptic transmission. © 2004 Wiley‐Liss, Inc.