Home Institution: UCLA
UCLA Mentor: Dr. Ketema Paul
Sleep is a state of mind and body that occurs in all animals and is regulated by sleep-wake homeostasis (Process S) and the circadian process (Process C). Non-rapid eye movement (NREM) sleep is characterized by high amplitude, low frequency cortical activity known as slow wave activity (SWA, 0.5-4.5 Hz) measured by electroencephalography (EEG). During NREM sleep thalamocortical projections become hyperpolarized, driving periods of highly synchronized activity in cortical neurons and giving rise to SWA. SWA is currently the best indirect metric for endogenous sleep pressure or “sleepiness” and thus the activity of Process S. Recent evidence suggests that two waveforms within SWA, slow oscillations (SOs) and delta waves (DWs), have distinct roles in memory consolidation, a sleep-dependent process (Kim et al., 2019); however, how these waveforms are affected by sleep pressure is unknown. We hypothesize that SOs during NREM (NREM SOs) may be a useful indicator of sleep pressure. Wildtype mice were implanted with EEG and electromyogram (EMG) recording electrodes (together “polysomnography”) to record periods of normal/undisturbed sleep pressure (baseline sleep) and artificially increased sleep pressure during 6 hours of acute sleep deprivation and the subsequent 18-hour recovery period. We found that NREM SOs and DWs occurred at significantly different numbers during the inactive phase but not during the active phase. Furthermore, we observed significant, unequal effects of acute sleep deprivation on NREM SOs and DWs during the recovery period. These findings suggest these waveforms may arise from separate physiological or behavioral contexts and warrant further investigation.