How Sleep Shapes Thalamocortical Circuit Function in the Visual System

Abstract

Recent data have shown that sleep plays a beneficial role for cognitive functions such as declarative memory consolidation and perceptual learning. In this article, we review recent findings on the role of sleep in promoting adaptive visual response changes in the lateral geniculate nucleus and primary visual cortex following novel visual experiences. We discuss these findings in the context of what is currently known about how sleep affects the activity and function of thalamocortical circuits and current hypotheses regarding how sleep facilitates synaptic plasticity.

Dynamical Mechanism Underlying Scale-Free Network Reorganization in Low Acetylcholine States Corresponding to Slow Wave Sleep

“…non-hub neurons with the least number of connections) exhibited a smaller magnitude of decrease in frequency in high-ACh state following the low-ACh state. Various in vivo studies have shown that SWS-mediated frequency dependent changes in firing rates within the visual cortex of mice led to the homogenization of spiking frequency of hippocampal neurons (Clawson et al, 2018;Durkin and Aton, 2019;Miyawaki et al, 2019).…”

Mutual interaction between Visual Homeostatic Plasticity and Sleep in Adult Humans

“…The artifact-free EEG segments analysed for estimating power band content in five frequency bands of interest were considered: theta (4-8 Hz), alpha (8)(9)(10)(11)(12), low beta (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30), high beta (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) and gamma (30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45). Power densities were estimated applying a Hammingwindowed FFT on 4 sec consecutive EEG segments and log-transformed (dB).…”

“…Importantly, this effect was specifically induced by sleep: two hours of dark exposure after MD did not prevent the decay of the effect. Results from animal models have shown that NREM sleep consolidates ocular dominance plasticity during the critical period 32,34,49 . This sleepdependent consolidation relies on Hebbian mechanisms and it is mediated by synaptic potentiation through increased NMDAR and PKA activity 32 and decreased GABAergic inhibition 34 .…”

“…Evidence from animal models shows that NREM sleep is necessary to consolidate Hebbian mechanisms during ocular dominance plasticity within the critical period [32][33][34] , however, it is still . CC-BY-NC-ND 4.0 International license available under a (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.…”

“…Evidence from animal models shows that NREM sleep is necessary to consolidate Hebbian mechanisms during ocular dominance plasticity within the critical period [32][33][34] , however, it is still largely unknown whether sleep has similar effects after the closure of the critical period and on homeostatic plasticity induced by MD. This is particularly important given that homeostatic plasticity is retained in the adult human brain [24][25][26]28,29,[35][36][37][38][39][40] .…”