Dependence of calcium influx in neocortical cells on temporal structure of depolarization, number of spikes, and blockade of NMDA receptors
✍ Scribed by Pavel Balaban; Marina Chistiakova; Aleksey Malyshev; Maxim Volgushev
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 367 KB
- Volume
- 76
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
Abstract
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.