Abstract
Sleep improves cognition and is necessary for normal brain plasticity, but the precise cellular and molecular mechanisms mediating these effects are unknown. At the molecular level, experience-dependent synaptic plasticity triggers new gene and protein expression necessary for long-lasting changes in synaptic strength.1 In particular, translation of mRNAs at remodeling synapses is emerging as an important mechanism in persistent forms of synaptic plasticity in vitro and certain forms of memory consolidation.2 We have previously shown that sleep is required for the consolidation of a canonical model of in vivo plasticity (i.e., ocular dominance plasticity [ODP] in the developing cat).3 Using this model, we recently showed that protein synthesis during sleep participates in the consolidation process. We demonstrate that activation of the mammalian target of rapamycin [mTOR] pathway, an important regulator of translation initiation,4 is necessary for sleep-dependent ODP consolidation and that sleep promotes translation (but not transcription) of proteins essential for synaptic plasticity (i.e., ARC and BDNF). Our study thus reveals a previously unknown mechanism operating during sleep that consolidates cortical plasticity in vivo.