Abstract

Synaptic scaling allows neurons to adjust synaptic strength in response to chronic alterations in neuronal activity. A new study in PLOS Biology identifies a pathway that synergizes protein synthesis and degradation with remodeling of the microRNA (miRNA)-induced silencing complex (miRISC) to mediate synaptic scaling.

Highlights

  • The mechanisms at play for the expression of synaptic scaling depend on the proteome remodeling [7] and result in changes in AMPA-type glutamate receptors at postsynaptic sites

  • Srinivasan and colleagues describe that concomitant inhibition of the proteasome and translation blocks synaptic downscaling and the decrease in surface AMPA receptors triggered upon prolonged neuronal hyperactivity, suggesting that the 2 processes cooperate to induce synaptic downscaling

  • To understand mechanistically how synaptic downscaling depends on proteomic remodelingAthUat:iAnvnoalbvbersebvoiathtiopnrloitsethinastrbaenesnlcaotimonpialenddfodretghroasdeautsieodnt,htrhoeuaguhtohuottrhseftoecxut:sPedleoasnetvheerifythatalle opposite changes in the expression levels and polysome association of 2 of the microRNA-induced silencing complex (miRISC) components, Trim32 and MOV10, triggered by chronic neuronal hyperactivity

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Summary

Introduction

The mechanisms at play for the expression of synaptic scaling depend on the proteome remodeling [7] and result in changes in AMPA-type glutamate receptors at postsynaptic sites. Srinivasan and colleagues explore the possibility that protein synthesis and degradation processes work in coordination to control homeostatic synaptic scaling of excitatory synapses [8].

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