Biophysical model of spike-timing-dependent plasticity based on temporal factors of intracellular Ca2+

In this study, we propose a biophysical plasticity model that incorporates the temporal factors of spine Ca2+ signals and demonstrates that spike-timing-dependent plasticity (STDP) is attributable to the Ca2+ entry through NMDA receptors (NMDARs). We also analyze the effects of the developmental change in NMDAR kinetics on the STDP curve. The results show that the change in NMDAR kinetics functions as a metaplasticity that contributes to potentiating immature synapses during early development.