Modulation of working memory duration by synaptic and astrocytic mechanisms

PLoS Comput Biol. 2022 Oct 3;18(10):e1010543. doi: 10.1371/journal.pcbi.1010543. eCollection 2022 Oct.

Abstract

Short-term synaptic plasticity and modulations of the presynaptic vesicle release rate are key components of many working memory models. At the same time, an increasing number of studies suggests a potential role of astrocytes in modulating higher cognitive function such as WM through their influence on synaptic transmission. Which influence astrocytic signaling could have on the stability and duration of WM representations, however, is still unclear. Here, we introduce a slow, activity-dependent astrocytic regulation of the presynaptic release probability in a synaptic attractor model of WM. We compare and analyze simulations of a simple WM protocol in firing rate and spiking networks with and without astrocytic regulation, and underpin our observations with analyses of the phase space dynamics in the rate network. We find that the duration and stability of working memory representations are altered by astrocytic signaling and by noise. We show that astrocytic signaling modulates the mean duration of WM representations. Moreover, if the astrocytic regulation is strong, a slow presynaptic timescale introduces a 'window of vulnerability', during which WM representations are easily disruptable by noise before being stabilized. We identify two mechanisms through which noise from different sources in the network can either stabilize or destabilize WM representations. Our findings suggest that (i) astrocytic regulation can act as a crucial determinant for the duration of WM representations in synaptic attractor models of WM, and (ii) that astrocytic signaling could facilitate different mechanisms for volitional top-down control of WM representations and their duration.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Astrocytes* / physiology
  • Memory, Short-Term* / physiology
  • Models, Neurological
  • Neuronal Plasticity / physiology
  • Synaptic Transmission

Grants and funding

This study was supported by the Max Planck Society (T.T.), the German Research Foundation via CRC1080 (T.T.) and its student-postdoc cooperation program (A.N. and S.B.), the Joachim Herz Foundation (Add-on fellowship, A.N.), Studienstiftung des deutschen Volkes (S.B.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.