Interplay of STDP and dendritic plasticity in a hippocampal CA1 pyramidal neuron model

Abstract

Synaptic plasticity in hippocampal CA1 pyramidal neurons is accompanied and shaped by dendritic plasticity, the long-lasting and region-specific alteration of the biophysical properties of voltage-gated dendritic ion channels. Down-regulation of A-type potassium current IA, observed after long-term potentiation induction, boosts the amplitude of somatic back-propagating action potentials and the associated calcium concentration in dendritic spines, increases the amplitude of the excitatory postsynaptic potentials and promotes synaptic integration. Using a detailed computational model of a CA1 pyramidal cell and a spiketiming-dependent synaptic plasticity (STDP) protocol we found that supression of A-type potassium current IA leads to the increased dendritic excitability converting long-term depression to long-term potentiation in proximal synapses and supporting fast Hebbian plasticity in distal synapses on a hippocampal CA1 pyramidal neuron. 1 Introduction. Biological neurons store memories not only in thei rsynapses, but also in the biophysical properties of dendritic ion channels. Long-term spike-timing-dependent synaptic plasticity (STDP) refers to the synaptic ability to modify its strenght depending on the temporal order of presynaptic and postsynaptic activity: if the presynaptic spike precedes the postsynaptic spike within a short time window, the synapse undergoes long-term potentiation (LTP), and it exhibits long-term depression (LTD) if the temporal order is reversed [2]. Physiological experiments show that induction of long-term synaptic plasticity is followed by a local increase in dendritic excitability in CA1 pyramidal neurons [4], [8], [9], [11]. Specifically, LTP is accompanied by a region-specific and long-lasting down-regulation of Atype potassium currentIA that leads to the boosted amplitude of the somatic back-propagating action potentials (bAPs), elevated calcium levels in dendrites and d[...].