Simplified calcium signaling cascade for synaptic plasticity
This work addresses the need for more realistic and simplified models of synaptic plasticity in neuroscience, offering a tangible alternative to conceptual theories, though it appears incremental as it builds on existing frameworks like the Bienenstock-Cooper-Munro theory.
The authors tackled the problem of modeling synaptic plasticity by proposing a simplified calcium signaling cascade based on tangible chemical reactions, which successfully reproduced experimental synaptic plasticity from protocols like synchronous pairing and correlated action potentials, as well as ocular dominance plasticity through synapse-specific back-propagating action potentials.
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.