Abstract

Since its discovery, spike timing-dependent synaptic plasticity (STDP) has been thought to be a primary mechanism underlying the brain’s ability to learn and to form new memories. However, despite the enormous interest in both the experimental and theoretical neuroscience communities in activity-dependent plasticity, it is still unclear whether plasticity rules inferred from in vitro experiments apply to in vivo conditions. Among the multiple reasons why plasticity rules in vivo might differ significantly from in vitro studies is that extracellular calcium concentration use in most studies is higher than concentrations estimated in vivo. STDP, like many forms of long-term synaptic plasticity, strongly depends on intracellular calcium influx for its induction. Here, we discuss the importance of considering physiological levels of extracellular calcium concentration to study functional plasticity.

Highlights

  • Spike timing-dependent plasticity (STDP) is a form of long-term synaptic modification thought to constitute a mechanism underlying formation of new memories

  • Analog-digital modulation of action potential-evoked synaptic transmission lies on modification of spike shape, by either broadening the axonal spike (Shu et al, 2006; Kole et al, 2007) or by modulating its amplitude (Rama et al, 2015; Zbili et al, 2020)

  • Dendritic integration or EPSP-Spike coupling is modified with synaptic changes (Campanac and Debanne, 2008)

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Summary

Introduction

Spike timing-dependent plasticity (STDP) is a form of long-term synaptic modification thought to constitute a mechanism underlying formation of new memories. In Hebbian STDP, the correlation between an EPSP and the backpropagated action potential (bAP) corresponding to a prebefore-post pairing that leads to t-LTP, induces large calcium entry (Koester and Sakmann, 1998). These two forms of plasticity which are dependent on post-synaptic NMDA receptors are found in the hippocampus at CA3-CA1 synapses of rodents (Nishiyama et al, 2000; Andrade-Talavera et al, 2016) or in the layer II/III of the cortex of rodents (Froemke et al, 2006).

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