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. Copyright 2004 Wiley-Liss, Inc.