Instantons in the working memory: implications for schizophrenia

TL;DR

This paper investigates how synaptic channel properties, especially NMDA receptor activity, influence the stability of working memory in neural networks, explaining memory deterioration in schizophrenia.

Contribution

It demonstrates the critical role of NMDA receptor-mediated EPSC in maintaining stable delayed activity and provides analytical and computational insights into memory decay mechanisms.

Findings

NMDA receptor channels support more reliable reverberating activity than AMPA.

Decay of delayed activity is driven by synaptic transmission unreliability.

Analytical and computational models confirm the decay mechanisms.

Abstract

The influence of the synaptic channel properties on the stability of delayed activity maintained by recurrent neural network is studied. The duration of excitatory post-synaptic current (EPSC) is shown to be essential for the global stability of the delayed response. NMDA receptor channel is a much more reliable mediator of the reverberating activity than AMPA receptor, due to a longer EPSC. This allows to interpret the deterioration of working memory observed in the NMDA channel blockade experiments. The key mechanism leading to the decay of the delayed activity originates in the unreliability of the synaptic transmission. The optimum fluctuation of the synaptic conductances leading to the decay is identified. The decay time is calculated analytically and the result is confirmed computationally.