Non-rapid eye movement sleep (NREMS) onset is characterized by a reduction in cerebral metabolism and an increase in slow waves, 1-4-Hz oscillations between relatively depolarized and hyperpolarized states in the cerebral cortex. The metabolic consequences of slow-wave activity (SWA) at the cellular level remain uncertain. We sought to determine whether SWA modulates the rate of glycolysis within the cerebral cortex. The real-time measurement of lactate concentration in the mouse cerebral cortex demonstrates that it increases during enforced wakefulness. In spontaneous sleep/wake cycles, lactate concentration builds during wakefulness and rapid eye movement sleep and declines during NREMS. The rate at which lactate concentration declines during NREMS is proportional to the magnitude of electroencephalographic (EEG) activity at frequencies of <10 Hz. The induction of 1-Hz oscillations, but not 10-Hz oscillations, in the electroencephalogram by optogenetic stimulation of cortical pyramidal cells during wakefulness triggers a decline in lactate concentration. We conclude that cerebral SWA promotes a decline in the rate of glycolysis in the cerebral cortex. These results demonstrate a cellular energetic function for sleep SWA, which may contribute to its restorative effects on brain function.
The anti-neuroinflammatory agent minocycline prevents either the buildup or expression of sleep need in rodents. The molecular mechanism underlying this effect is not known, but it is not mediated by suppression of il-1β, il-6, and tnfα at the transcript level.
Markers of sleep drive (<10Hz; slow wave activity and theta) have been identified in the course of slow wave sleep (SWS) and wakefulness. So far, higher frequencies in the waking electroencephalogram have not been examined thoroughly as a function of sleep drive. Here, we measured EEG dynamics in epochs of active wake (AW; wake characterized by high muscle tone) or quiet wake (QW; wake characterized by low muscle tone). We hypothesized that the higher beta oscillations (15-35Hz, measured by local field potential and electroencephalography) represent fundamentally different processes in AW and QW.
In AW, sensory-stimulation elevated beta activity in parallel with gamma (80-90Hz) activity, indicative of cognitive processing. In QW, beta activity paralleled slow wave activity (1-4Hz) and theta (5-8Hz) in tracking sleep need. Cerebral lactate concentration, a measure of cerebral glucose utilization, increased during AW whereas it declined during QW. Mathematical modeling of state-dependent dynamics of cortical lactate concentration was more precisely predictive when QW and AW were included as two distinct substates rather than a uniform state of wakefulness. The extent to which lactate concentration declined in QW and increased in AW was proportionate to the amount of beta activity.
These data distinguish QW from AW. QW, particularly when characterized by beta activity, is permissive to metabolic and electrophysiological changes that occur in SWS. These data urge further studies on state dependent beta oscillations across species.
These data demonstrate that innate immune signaling pathways active in the monocyte lineage, including presumably microglia, detect and mediate in part the cerebral reaction to sleep loss.
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