Neurogenesis and multiple plasticity mechanisms enhance associative memory retrieval in a spiking network model of the hippocampus

TL;DR

This paper presents a large-scale, biologically plausible spiking neural network model of the hippocampus that demonstrates how neurogenesis and plasticity mechanisms improve associative memory encoding and retrieval.

Contribution

It is the first to model hippocampal memory with significantly more neurons and to investigate the role of neurogenesis in memory processes within such a model.

Findings

Neurogenesis maintains CA3 neuron recruitment per memory, aiding recent memory retrieval.

Plasticity models are crucial for effective memory encoding and retrieval.

Structural plasticity is necessary for memory function when the network is overloaded.

Abstract

Hippocampal CA3 is crucial for the formation of long-term associative memory. It has a heavily recurrent connectivity, and memories are thought to be stored as memory engrams in the CA3. However, despite its importance for memory storage and retrieval, spiking network models of the CA3 to date are relatively small-scale, and exist as only proof-of-concept models. Specifically, how neurogenesis in the dentate gyrus affects memory encoding and retrieval in the CA3 is not studied in such spiking models. Our work is the first to develop a biologically plausible spiking neural network model of hippocampal memory encoding and retrieval, with at least an order-of-magnitude more neurons than previous models. It is also the first to investigate the effect of neurogenesis on CA3 memory encoding and retrieval. Using such a model, we first show that a recently developed plasticity model is crucial for good encoding and retrieval. Next, we show how neural properties related to neurogenesis and neuronal death enhance storage and retrieval of associative memories in the CA3. In particular, we show that without neurogenesis, increasing number of CA3 neurons are recruited by each new memory stimulus, resulting in a corresponding increase in inhibition and poor memory retrieval as more memories are encoded. Neurogenesis, on the other hand, maintains the number of CA3 neurons recruited per stimulus, and enables the retrieval of recent memories, while forgetting the older ones. Our model suggests that structural plasticity (provided by neurogenesis and apoptosis) is required in the hippocampus for memory encoding and retrieval when the network is overloaded; synaptic plasticity alone does not suffice. The above results are obtained from an exhaustive study in the different plasticity models and network parameters.