Sleep and sleep optimization have been areas of interest for years. People seek to learn how to maximize their sleep, what constitutes “good” sleep, and the long-term effects of poor sleep. One such researcher in this field, Dr. Stephanie Crowley, delivered a talk this semester about the effects and potential causes of poor sleep among adolescents. As children grow, their circadian rhythms shift later and later, their “biological night” shifting back much farther into the evening. This shift in sleep schedule, coupled with various sources of pressure, creates what Dr. Crowley dubs a “perfect storm” of chronic sleep deprivation. According to the work of Dr. Crowley, such sources include early school start times that are incongruous with their later biological schedule; social stressors; and an increased sensitivity to evening light that makes it more difficult yet to fall asleep.
It is believed that sleep quality and sleep schedules are generally regulated by two components: the circadian system and the homeostatic system. The circadian system cycles approximately every 24 hours and is generally consistent regardless of prior sleep/wake conditions. It is more dependent on the time of day and exposure to light. In contrast, its counterpart, the homeostatic system, is quite dependent on prior sleep/wake conditions. It favors sleep the longer one is awake, and favors wakefulness if one has been asleep for a sufficient period. What is most fascinating is the seemingly multimodal nature of the homeostatic system. The circadian system has been localized to the suprachiasmatic nucleus of the hypothalamus; the homeostatic system, however, does not have a single localized center. Instead, it is hypothesized that it synthesizes inputs from many areas of the brain, including but not limited to the nucleus of the solitary tract; the parabrachial nucleus; GABAergic neurons in the medulla; cholinergic neurons in the nucleus ambiguous; and catecholaminergic cells in the ventrolateral medulla and locus coeruleus that work together to regulate sleep-wake states.
Each of these areas interfaces with the others to promote restful sleep and regulate arousal in the event of danger while one is asleep. For example, the parabrachial nucleus, which serves as the brain’s alarm system and receives inputs from the NST, is primarily known for its arousal-promoting functions. However, a subset of PBN neurons—Adycap1-expressing NST-to-PBN projections—directly promote NREM sleep, thus implicating it as having a much more significant role in sleep-wake regulation. Additionally, the norepinephrinergic locus coeruleus neurons found in the dorsal pons are highest during active wakefulness and absent during REM sleep. The activity of these neurons is crucial for regulating attention and arousal, but sleep-promoting neurons can suppress them via GABAergic inhibition.
The homeostatic system needs many parts to function as smoothly as it does. As someone keen on learning and memory, it would be very interesting to find out the downstream effects of the dysfunction of these areas of the brain, as it has been long established that chronically poor sleep impairs both.
Works Cited
Yao, Yuanyuan, and Yang Dan. “Body-Brain Integration: The lower brainstem in sleep-wake regulation.” Annual Review of Neuroscience, 20 Apr. 2026, https://doi.org/10.1146/annurev-neuro-082625-012115.
Crowley, Stephanie J., et al. “An update on adolescent sleep: New evidence informing the perfect storm model.” Journal of Adolescence, vol. 67, no. 1, 13 June 2018, pp. 55–65, https://doi.org/10.1016/j.adolescence.2018.06.001.
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