Homeostatic scaling in neurons has been majorly attributed to the individual contribution of either translation or degradation; however there remains limited insight towards understanding how the interplay between the two processes effectuates synaptic homeostasis. Here, we report that a co-dependence between the translation and degradation mechanisms drives synaptic homeostasis whereas abrogation of either prevents it. Coordination between the two processes is achieved through the formation of a tripartite complex between translation regulators, the 26S proteasome and the miRNA-induced-silencing-complex (miRISC) components such as MOV10 and Trim32 on actively translating transcripts or polysomes. Disruption of polysomes abolishes this ternary interaction, suggesting that translating RNAs facilitate the combinatorial action of the proteasome and the translational apparatus. We identify that synaptic downscaling involves miRISC remodelling which entails the mTOR-dependent translation of Trim32, an E3 ligase and the subsequent degradation of its target, MOV10. MOV10 degradation is sufficient to invoke downscaling by enhancing Arc expression and causing the subsequent removal of post-synaptic AMPA receptors. We propose a mechanism that exploits a translation-driven degradation paradigm to invoke miRISC remodelling and induce homeostatic scaling during chronic network activity. ### Competing Interest Statement The authors have declared no competing interest.