Electrical and metabolic markers of sleep

Derrick James Phillips

Traditional methods for scoring sleep may be inadequate under pathological or abnormal conditions. Electrical and metabolic markers of sleep may provide better metrics for identifying sleep state. We used electrophysiology measurements combined with spectroscopic imaging techniques to record neural and hemodynamic responses to auditory stimuli in rats. Varying intensity auditory stimuli were produced to measure evoked electrical and hemodynamic activity. Initially, we determined if low-level intermittent auditory stimuli have the potential to disrupt sleep during 24-h recordings by assessing arousal occurrence. Additionally, if stimulusgenerated auditory evoked response potential (AEP) components provide a metric of underlying cortical state, then a particular AEP structure may precede an arousal. Next, to investigate statedependent modulation of stimulus intensity response profiles within different brain structures, we assessed AEP components across both stimulus intensity and state. We found that low-level auditory stimuli did not fragment animal sleep since we observed no significant change in arousal occurrence. Arousals that occurred within 4s of a stimulus exhibited AEP mean area and latency features similar to AEPs generated during wake, indicating that the underlying cortical tissue state may contribute to physiological conditions required for arousal. Stimulation intensity and the corresponding AEP response profile were dependent on both brain structure and sleep state. Lower brain structures maintained stimulus intensity and neural response relationships during sleep. This relationship was not observed in the cortex, implying state-dependent modification of stimulus intensity coding. Finally, we measured neural and hemodynamic responses following different amounts of sleep deprivation. Following 10hrs of deprivation, evoked hemodynamic amplitudes during quite sleep (QS) were blunted, while evoked electrical amplitudes increased. Steady state HbO2 concentration increased during 10hrs of deprivation and remained high during the initial recovery period before returning to baseline levels after 12hrs. Sleep deprivation may drive the vasculature to its expansion limit, as indicated by a blunted hemodynamic response and high steady state HbO2 levels. Decreased neural activity during recovery sleep may allow blood vessel compliance to return to a baseline level. Chronic sleep deprivation or sleep restriction could push the vasculature to critical levels, which may lead to metabolic syndromes and neural deficits.

Electrical and metabolic markers of sleep

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