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
Summary
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].
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have