| Abstract No.: | B-B2036 |
| Country: | Canada |
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| Title: | SPIKE-DEPENDENT SYNAPTIC FEEDBACK IN CORTICAL PYRAMIDAL NEURONS |
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| Authors/Affiliations: | 1 Jean-François Boucher*; 1 Josée Seigneur; 1 Igor Timofeev;
1 Université Laval, Québec, QC, Canada
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| Content: | Background. Action potentials (AP) induce voltage-gated inward calcium currents (VGCCs). Liberation of neurotransmitters is mediated by the inflow of calcium in presynaptic terminations, thus allowing liberation of the neurotransmitters in the synaptic cleft. We hypothesized that AP activation of VGCCs can modify the external concentration of calcium around the dendrites of postsynaptic neurons strongly enough to affect the release of neurotransmitters.
Methods. The whole-cell recordings from pyramidal cortical neurons of layers 2-3 were done in current- and voltage clamp (IC and VC) mode in rat brain slices maintained in vitro. APs in recorded neuron were elicited by either current injection in current-clamp mode or they were voltage imposed in voltage-clamp mode. Synaptic stimulation was achieved using tungsten microelectrodes located in the vicinity of the recorded neuron. The intensity of extracellular stimulation was adjusted to record both responses (EPSPs) and failures in the postsynaptic neuron in control and the stimuli were applied with delays of 10, 20, 40, 60, 80 and 100ms after AP.
Results. APs or voltage steps to +20 mV were followed by a prolonged afterhyperpolarization (AHP) in IC recordings or a strong outward current in VC recordings. In IC we observed a significant increase in failure rates only at 10ms after the AP. The increase in failure rates was not recorded in VC experiments. Such a difference could be explained by AHP-related shunting in IC recordings and our inability to detect responses in this experimental setup. In the following experiments we stimulated postsynaptic neurons with bursts of 4 APs spaced by 15 ms. Using this protocol, we obtained an increase in failure rates lasting at least 40ms in both IC and VC recordings.
Conclusion. We conclude that, in neocortex, the bursts of APs significantly decrease the release probability of presynaptic neurons. This likely occurs due to extracellular Ca2+ depletion associated with neuronal firing. Therefore, bursts of APs reduce the ability of neuron to respond to incoming synaptic volleys.
Supported by CIHR and NSERC.
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