Possible Modulation of Spike-Timing-Dependent Plasticity by Cholinergic Input in a Hippocampal CA3 Pyramidal Cell Model

Abstract—During rest in a maze task, place cells of the rat hippocampus are activated in the forward or reverse direction of the pathway. The synaptic plasticity of the place cells contributes to those activations. As acetylcholine suppresses synaptic connection between pyramidal cells, synaptic plasticity during the maze task requires considering temporal changes in theta rhythm and acetylcholine concentration. In the present study, we investigated the formation of synaptic connections between place cells in the hippocampal CA3 network model in response to fluctuations in acetylcholine concentrations with theta rhythm. First, paired-pulse simulations showed that the acetylcholine modulation of synaptic currents induced symmetric or asymmetric spike-timing-dependent plasticity. Second, in a linear track running, intracellular Ca2+ concentration-dependent synaptic plasticity as a neural basis formed the asymmetric synaptic connection distribution in which synaptic connection weights between place cells are potentiated along the direction of travel and attenuated in the opposite direction. The results suggest that such asymmetric potentiation of synaptic connections between place cells leads to unidirectional spike propagation along the pathway.