Protein Synthesis during SleepConsolidates Cortical Plasticity In Vivo
2012
Sleep consolidates experience-dependent brain plasticity,
but the precise cellular mechanisms mediating this process
are unknown [1]. De novo cortical protein synthesis is one
possible mechanism. In support of this hypothesis, sleep
is associated with increased brain protein synthesis [2, 3]
and transcription of messenger RNAs (mRNAs) involved in
protein synthesis regulation [4, 5]. Protein synthesis in
turn is critical for memory consolidation and persistent
forms of plasticity in vitro and in vivo [6, 7]. However, it is
unknown whether cortical protein synthesis in sleep serves
similar functions. We investigated the role of protein
synthesis in the sleep-dependent consolidation of a classic
form of cortical plasticity in vivo (ocular dominance plasticity,
ODP; [8, 9]) in the cat visual cortex. We show that
intracortical inhibition of mammalian target of rapamycin
(mTOR)-dependent protein synthesis during sleep abolishes
consolidation but has no effect on plasticity induced
during wakefulness. Sleep also promotes phosphorylation
of protein synthesis regulators (i.e., 4E-BP1 and eEF2) and
the translation (but not transcription) of key plasticity related
mRNAs (ARC and BDNF). These findings show that sleep
promotes cortical mRNA translation. Interruption of this
process has functional consequences, because it abolishes
the consolidation of experience in the cortex.
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