According to the synaptic homeostasis hypothesis of Tononi and Cirelli (Sleep Med Rev 10(1):49–62, 2006), the homeostatic regulation of sleep slow wave activity is related to the amount of the synaptic potentiation that has accumulated during the preceding waking state. The homeostatic increase of slow wave activity is shown to be valid for regional involvement in special localization related tasks, especially true for the frontal lobe.
High synaptic potentiation characterizes the early childhood’s abundant plastic changes when sleep contains high amounts of delta activity, while the decrease of potentiation in the elderly is associated with important decrease of sleep slow waves, nicely supporting the hypothesis.
According to this hypothesis, slow waves promote a generalized depression or downscaling of synaptic strength reached during wakefulness. Very much in congruence with the hypothesis, it was found that the cerebral blood flow is low in the morning after a night sleep compared to the end of a waking day, as measured by H215O PET studies. Furthermore, the blood flow values proved to be less and less parallel with the decrease of slow wave activity along the sleep cycles.
Sleep deprivation results in well-known negative cognitive symptoms. That also fits into the hypothesis because of the synaptic overload without the possibilities of downscaling because of the lack of sleep.
A close relationship between the amount of sleep slow wave activity and the cognitive performances in different human pathological conditions also supports the hypothesis.
Sleep deprivation mimics the prefrontal symptoms of mental deterioration in the elderly, where the rebound in frontal delta activity after sleep deprivation is missing. Another aspect of the relationship between human cognitive functions and sleep slow wave activity is that disorders like sleep apnea, Alzheimer disease, or insomnia, all associated with different degree of cognitive decline, show impairment of both NREM sleep and frontal slow wave activity.
The evidences about the importance of NREM slow wave activity in cognitive functions explains the interest about the role of CAP A1 phenomenon in cognition. We present here studies pointing to relationship between cognitive employment and CAP A1 type amount during the next night sleep. These preliminary results again connect input-dependent slow wave regulation with the use of dependent long-term homeostatic regulation.
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