A model and simulation research of NMDA-depended bidirectional synaptic plasticity

AIM:To study the correlative mechanism be-tween the induction of long term modification and the activityof different NMDA receptor subtypes.METHODS:Basedon the analysis of dynamic properties of NMDA receptorsubtypes, an amended mathematical model of postsynapticcalcium was proposed to describe the relationship betweendifferent NMDA receptor subtype activity and presynapticstimulus frequency. Along with a biochemical-reaction net-works model of the postsynaptic Ca2 +-depended signalingpathways, we developed a unified biophysical model aboutthe hippocampal CA3-CA1synapses bidirectional plasticity.RESULTS:According to the inductive condition of long-termpotentiation (LTP) and long term depression (LTD), ourcomputer simulation mimicked the induction processes ofNMDAR-dependent long term modification.CONCLU-SION:It is elucidated that the calcium transients requiredfor LTD may primarily come from the calcium inflow media-ted by NR2B subtype channel of NMDA receptor and the in-duction of LTP may require the calcium inflow mediated byNR2B subtype channel.