Homeostatic Plasticity in Primary Visual Cortex Affects Local Sleep Expression: A High-Density EEG

Introduction: Sleep and plasticity are highly interrelated. Plasticity in primary visual cortex (V1) can be induced in adults by short-term monocular deprivation. This manipulation temporarily increases ocular dominance for the deprived eye. This form of plasticity is mediated by a reduction of GABAergic inhibition in V1. Sleep unconsciousness is the price to pay for affording brain plasticity. Sleep Slow Oscillations (SSOs), i.e. alternations between states of hyperpolarization and synaptic activity of cortical neurons, are EEG graphoelements underlying respectively unconsciousness and plasticity. In vitro models pointed out that SSOs are modulated by cortical GABA levels. The aim is to find an in vivo signature of visual cortical plasticity, induced by short-term monocular deprivation, in the expression of SSOs in V1 during subsequent sleep. Methods: Fifteen healthy volunteers underwent 2h-monocular deprivation before going to sleep. The change in ocular dominance was measured before sleep using a binocular rivalry paradigm (Deprivation Index, DI). SSOs were detected with high-density EEG, and analysed in comparison with SSOs detected during a control night (without monocular deprivation). Results: Short-term monocular deprivation is associated, over occipital areas, with increased SSO amplitude and slope in the upward transition from hyperpolarization (p<0.05). In the same areas, volunteers more susceptible to monocular deprivation (lower DI) showed greater increases in SSO amplitude (correlation with DI: r=-0.75, p<0.05) and in upward transition slope (r=-0.65 p<0.05) after short-term monocular deprivation, compared to control night. Conclusion: The induction of visual cortical plasticity modulates SSOs in adult human, probably reflecting changes of GABAergic inhibition.