Simplified calcium signaling cascade for synaptic plasticity. (March 2020)

• Record Type: Journal Article
• Authors: Kornijcuk, Vladimir; Kim, Dohun; Kim, Guhyun; Jeong, Doo Seok
• Is Part Of: Neural networks. Volume 123(2020)
• Page Start: 38
• Page End: 51
• Publication Date: 2020-03
• Subjects: Synaptic plasticity -- Calcium signaling cascade -- Back-propagating action potential boost -- Synaptic competition; Neural computers -- Periodicals; Neural networks (Computer science) -- Periodicals; Neural networks (Neurobiology) -- Periodicals; Nervous System -- Periodicals; Ordinateurs neuronaux -- Périodiques; Réseaux neuronaux (Informatique) -- Périodiques; Réseaux neuronaux (Neurobiologie) -- Périodiques; Neural computers; Neural networks (Computer science); Neural networks (Neurobiology); Periodicals; 006.32
• DOI: 10.1016/j.neunet.2019.11.022
• Languages: English
• ISSNs: 0893-6080

Abstract

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 C 1 and C 2 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.