The Role Of Rem Sleep In Ocular Dominance Plasticity Consolidation

Despite decades of research, the function of sleep remains controversial. One theory is that sleep plays a role in consolidating plasticity induced during prior waking. Ocular dominance plasticity (ODP) in the cat visual cortex is induced during waking monocular deprivation (MD) and consolidated during subsequent sleep. Extracellular signal-regulated kinase (ERK) signaling is required for ODP and is elevated during post-MD sleep, but its requirement during sleep is unknown. In Chapter 2, we investigated whether ERK activity is required during sleep for ODP consolidation by inhibiting the upstream activator of ERK (MEK) with intracortical infusions of U0126 into V1 during post-MD sleep. ERK inhibition abolished ODP consolidation, as measured by extracellular single unit recording. Furthermore, ERK inhibition reduced phosphorylation of eukaryotic initiation factor 4E (eIF4E) and post-synaptic density protein 95 (PSD-95) levels. MAP kinase-interacting kinase 1 (Mnk1) is activated by ERK and directly phosphorylates eIF4E; inhibition of Mnk1 mimicked the effects of ERK inhibition. These results show that activation of the ERK-Mnk1 pathway during post-MD sleep is required for ODP consolidation, and that this pathway promotes the synthesis of plasticity-related proteins such as PSD-95. However, sleep can be broadly subdivided into rapid eye movement (REM) and non-REM (NREM) sleep, but the relative contributions of these states to ODP and the ERK pathway ar