Related to synaptic plasticity, we recently unraveled a mechanism governing the de novo translation and synaptic incorporation of GluA1-containing AMPA receptors upon activity deprivation, a process called homeostatic synaptic scaling.
This novel mechanism involves a regulation by microRNA-92a, which selectively represses the local translation of GluA1 by binding its 3’UTR. MiR-92a is downregulated in conditions of synaptic silencing and its over-expression blocks GluA1-mediated upscaling (Letellier et al., Nat Neurosci 2014). This study involving GluA1 immunocytochemistry, and patch-clamp recordings of miniature AMPA currents (right), was performed in collaboration with A. Favereaux (team Landry), a specialist of micro-RNAs. We are currently identifying novel micro-RNAs regulating Nlg expression in conditions of chronic activity blockade.