Abstract

Synaptic efficacy is subjected to activity-dependent changes on short- and long time scales. While short-term changes decay over minutes, long-term modifications last from hours up to a lifetime and are thought to constitute the basis of learning and memory. Both plasticity mechanisms have been studied extensively but how their interaction shapes synaptic dynamics is little known. To investigate how both short- and long-term plasticity together control the induction of synaptic depression and potentiation, we used numerical simulations and mathematical analysis of a calcium-based model, where pre- and postsynaptic activity induces calcium transients driving synaptic long-term plasticity. We found that the model implementing known synaptic short-term dynamics in the calcium transients can be successfully fitted to long-term plasticity data obtained in visual- and somatosensory cortex. Interestingly, the impact of spike-timing and firing rate changes on plasticity occurs in the prevalent firing rate range, which is different in both cortical areas considered here. Our findings suggest that short- and long-term plasticity are together tuned to adapt plasticity to area-specific activity statistics such as firing rates.

Highlights

  • The impact of presynaptic action potentials on the postsynaptic neuron’s excitability varies on multiple time-scales; successive presynaptic spikes produce short-term depression or facilitation lasting for a few minutes, while prolonged pre- and postsynaptic stimulation induce longterm plasticity

  • We find that short- and longterm plasticity are tuned together such that the sensitive range of synaptic plasticity is located at firing rate ranges, which match the prevalent firing rates in the respective cortical regions

  • In order to study the interplay between short-term depression (STD) and long-term plasticity, we first extracted the short-term depression dynamics of postsynaptic responses for visualand somatosensory cortex

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Summary

Introduction

The impact of presynaptic action potentials on the postsynaptic neuron’s excitability varies on multiple time-scales; successive presynaptic spikes produce short-term depression or facilitation lasting for a few minutes, while prolonged pre- and postsynaptic stimulation induce longterm plasticity. Experimental studies have shown that the induction of synaptic long-term potentiation (LTP) and depression (LTD) depends on (i) the firing rates of pre- and postsynaptic neurons [1, 2] and on (ii) the precise timing of pre- and postsynaptic action potentials [3,4,5,6]. A dynamic enhancement of the postsynaptic reponse is termed shortterm facilitation and the reduction is called short-term depression (STD). Activity-dependent depression dominates synaptic transmission between neocortical pyramidal neurons [13]. The role of short-term synaptic changes for long-term plasticity induction has attracted little attention

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