Study objectives: Sleep slow-wave activity (SWA, electroencephalogram [EEG] power between 0.5 and 4.0 Hz) is homeostatically regulated, increasing with wakefulness and declining with sleep. Sleep SWA is thought to reflect sleep need, but the mechanisms of its homeostatic regulation remain unknown. Based on a recent hypothesis, we sought to determine whether a decrease in cortical synaptic strength can account for changes in sleep SWA.
Design: A large-scale computer model of the sleeping thalamocortical system was used to reproduce in detail the cortical slow oscillations underlying EEG slow waves.
Setting: N/A.
Patients or participants: N/A.
Interventions: Simulated reductions in the strength of corticocortical synapses.
Measurements and results: Decreased synaptic strength led to (1) decreased single cell membrane potential oscillations and reduced network synchronization, (2) decreased rate of neural recruitment and decruitment, and (3) emergence of local clusters of synchronized activity. These changes were reflected in the local EEG as (1) decreased incidence of high-amplitude slow waves, (2) decreased wave slope, and (3) increased number of multipeak waves. Spectral analysis confirmed that these changes were associated with a decrease in SWA.
Conclusions: A decrease in cortical synaptic strength is sufficient to account for changes in sleep SWA and is accompanied by characteristic changes in slow-wave parameters. Experimental results from rat cortical depth recordings and human high-density EEG show similar changes in slow-wave parameters with decreasing SWA, suggesting that the underlying mechanism may indeed be a net decrease in synaptic strength.