miR-92a regulates translation and synaptic incorporation of GluA1 containing AMPA receptors during homeostatic scaling
Nat Neurosci. 2014 - Jul 13. doi: 10.1038/nn.3762. [Epub ahead of print]
Mathieu Letellier1,2,*, Sara Elramah1,2,*, Magali Mondin1,2,*, Anaïs Soula1,2, Andrew Penn1,2, Daniel Choquet1,2, Marc Landry1,2, Olivier Thoumine1,2,$, Alexandre Favereaux1,2,$
MicroRNAs (miRNAs) are small non-coding RNAs that inhibit protein translation by binding to the 3′ untranslated region (3′ UTR) of target mRNAs. miRNAs are abundant in the brain, with the challenge being to identify their roles and targets in specific neuronal functions. Homeostatic synaptic scaling is a form of plasticity by which neurons make compensatory adjustments to the strength of excitatory synapses according to their activity level. Notably, postsynaptic AMPA receptors (AMPARs), which are the major effectors of communication at glutamatergic synapses, are upregulated following activity blockade. In a well-characterized procedure, treatment of hippocampal neurons with tetrodotoxin (TTX, to prevent action potentials) and AP5 (to further block NMDA receptor–mediated miniature synaptic transmission) increases the expression of GluA1 homomeric AMPARs through local translation of GluA1 mRNAs present in dendrites.