Simplified calcium signaling cascade for synaptic plasticity

TL;DR

This paper introduces a simplified calcium signaling model for synaptic plasticity that captures experimental results and competitive synaptic interactions without complex threshold-based assumptions.

Contribution

The model uses tangible chemical reactions to represent long-term plasticity, providing a more biochemical basis than previous conceptual threshold models.

Findings

Successfully reproduces experimental synaptic plasticity protocols

Models ocular dominance plasticity consistent with BCM theory

Demonstrates synapse competition via back-propagating action potentials

Abstract

We propose a model for synaptic plasticity based on a calcium signaling cascade. The model simplifies the full signaling pathways from a calcium influx to the phosphorylation (potentiation) and dephosphorylation (depression) of glutamate receptors that are gated by fictive C1 and C2 catalysts, respectively. This model is based on tangible chemical reactions, including fictive catalysts, for long-term plasticity rather than the conceptual theories commonplace in various models, such as preset thresholds of calcium concentration. Our simplified model successfully reproduced the experimental synaptic plasticity induced by different protocols such as (i) a synchronous pairing protocol and (ii) correlated presynaptic and postsynaptic action potentials (APs). Further, the ocular dominance plasticity (or the experimental verification of the celebrated Bienenstock--Cooper--Munro theory) was reproduced by two model synapses that compete by means of back-propagating APs (bAPs). The key to this competition is synapse-specific bAPs with reference to bAP-boosting on the physiological grounds.