A nonlinear cable framework for bidirectional synaptic plasticity.

Nicolangelo Iannella,Derek Abbott,Shigeru Tanaka,Thomas Launey,William Phillips

doi:10.1371/journal.pone.0102601

Abstract

Finding the rules underlying how axons of cortical neurons form neural circuits and modify their corresponding synaptic strength is the still subject of intense research. Experiments have shown that internal calcium concentration, and both the precise timing and temporal order of pre and postsynaptic action potentials, are important constituents governing whether the strength of a synapse located on the dendrite is increased or decreased. In particular, previous investigations focusing on spike timing-dependent plasticity (STDP) have typically observed an asymmetric temporal window governing changes in synaptic efficacy. Such a temporal window emphasizes that if a presynaptic spike, arriving at the synaptic terminal, precedes the generation of a postsynaptic action potential, then the synapse is potentiated; however if the temporal order is reversed, then depression occurs. Furthermore, recent experimental studies have now demonstrated that the temporal window also depends on the dendritic location of the synapse. Specifically, it was shown that in distal regions of the apical dendrite, the magnitude of potentiation was smaller and the window for depression was broader, when compared to observations from the proximal region of the dendrite. To date, the underlying mechanism(s) for such a distance-dependent effect is (are) currently unknown. Here, using the ionic cable theory framework in conjunction with the standard calcium based plasticity model, we show for the first time that such distance-dependent inhomogeneities in the temporal learning window for STDP can be largely explained by both the spatial and active properties of the dendrite.

Highlights

Countless experiments have shown that neural activity can modify the efficacy or weight of a synaptic connection between two neurons
The calcium dependent plasticity (CaDP) model, originally proposed by [45], is extended to take into account the spatial nature of the dendrite, and where alterations to synaptic strength are driven by calcium entry through voltage-dependent calcium channels and NMDA receptors
In the original model by Shouval et al [45], plastic change occurs through a single point of association that relies upon the interaction between glutamatergic NMDA receptor activation and strong depolarization of the postsynaptic membrane, where NMDA acts as a coincidence detector of pre- and postsynaptic activity

Summary

Introduction

Countless experiments have shown that neural activity can modify the efficacy or weight of a synaptic connection between two neurons. Landmark experiments have demonstrated that the precise timing and temporal order between presynaptic input and postsynaptic action potential generation dictates whether a synapse’s efficacy is potentiated or depressed [14,15,16,17,18,19]. An asymmetric temporal window is found emphasizing that if a presynaptic input precedes the generation of a postsynaptic action potential, the synapse is strengthened; but if the temporal order is reversed, depression results This type of plasticity is called spike timing-dependent plasticity (STDP) [14,18]

Methods

Results

Discussion

Conclusion