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

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.

journal_name

J Neurosci Res

authors

Balaban P,Chistiakova M,Malyshev A,Volgushev M

doi

10.1002/jnr.20104

keywords:

subject

Has Abstract

pub_date

2004-05-15 00:00:00

pages

481-7

issue

4

eissn

0360-4012

issn

1097-4547

journal_volume

76

pub_type

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