IV. SLEEP-SPECIFIC ELECTRICAL OSCILLATIONS
Neocortical slow oscillations and SWA, thalamo-cortical spindles and hippocampal SW-R have been associated with processes of memory consolidation during SWS and might support the reactivation and redistribution of memory representations during this sleep stage.
Virtually every corti- cal neuron, both excitatory as well as inhibitory neuron, engages in the slow oscillation with the firing patterns showing high synchrony across cellular populations
The widespread synchronization of cortical and thalamo-cortical networks during non-REM sleep is considered the major function of the slow oscillation, providing a global time frame whereby the net- work is clocked and reset by the hyperpolarizing phase and neuronal processing is limited to the subsequent de- polarizing up-phases
Synchronization of activity during depolarizing states might be partially achieved via corticocortical glutamatergic synaptic connections, implementing contributions of NMDA and AMPA receptor activation to establish long-range synchrony
Slow oscillations originating from thalamo-cortical neurons (586) vanish when the thalamus is isolated from cortical inputs (1200), indicating the slow oscillation is a primary cortical phenomenon
indicate that the slow oscillation behaves like a travelling wave, which originates most fre- quently in the frontal regions and propagates towards pos- terior regions, although other origins and directions of propagation occur
the largest slow waves (140 V) were associated with activation in the parahippocampal gyrus, cerebellum, and brain stem, whereas smaller waves were more related to activation changes in frontal areas
evidence that SWA and the slow oscillations represent a central mechanism conveying the beneficial effect of SWS on memory consolidation, in particular in the declarative memory system
In humans, intense learning of declarative memories (word pairs) enhanced amplitudes of the slow oscillation up-states as well as coherence in the SWA frequency band during succeeding SWS
slopes of the down-to-up state of the slow oscillations were steeper after learning.
Increases in local SWA were even observed when learning took place in the morning, suggesting that the training- induced changes in SWA do not depend on the time between training and subsequent sleep
SWA (as well as the amplitude and down-to-up state slope of the slow oscillation during SWS) reflect the intensity and amount of encoding during prior wakefulness, with some studies also indicating an association of these measures with later retrieval.
neuromodulatory milieu during SWS is characterized by low levels of acetylcholine, norepi- nephrine, and serotonin and therefore favors processes of depotentiation.
nice to know, aber kommt nicht rein
decrease in SWA across sleep reflects differences in the ho- meostatic regulation between 1 Hz slow oscillations and 1–4 Hz delta oscillations (6, 171, 1207). However, as dis- tinct qualitative differences between both frequency bands have not been confirmed, the decrease in SWA across sleep appears to be most parsimoniously explained by a decrease in the incidence of high-amplitude slow waves
GENETIC APPROACHES TO SLEEP-DEPENDENT MEMORY FORMATION
Sleep is genetically controlled
see also
Tags: neuroscience science
Superlink: 050 🧠Neuroscience
Sleep, Schlaf
Memory in Sleep
Source
Paper “About sleep’s role in memory” by Rasch, Björn from 2013
Created: 30-01-24 12:27