Dr. Paul’s lab focuses on the study of the genes, molecules, and hormones that influence sleep and wakefulness. Detrimental sleep-wake patterns that arise from daily environmental and social challenges increase the risk for cerebrovascular disease, cardiovascular disease, and metabolic syndrome. Though many of the neural circuits and hormonal axes that drive sleep and wakefulness have been identified, the specific role of neurons and hormones in facilitating the adverse effects of poor sleep remains ambiguous.

The hypothalamus, which is responsible for the homeostatic control of endocrine and metabolic function, governs sleep by: 1) generating the daily circadian rhythm of sleep and wakefulness and consolidating sleep-wake patterns during the night and day, 2) coordinating forebrain and hindbrain control of sleep and wake states, and 3) managing the pituitary hormones that modulate sleep and wakefulness in response to endogenous and exogenous pressures. In our lab, we study how the hypothalamic nuclei that regulate sleep promote and respond to the deleterious effects of extended wakefulness and stress in mice. We accomplish this by recording sleep-wake states in genetic and mutant mouse models of abnormal sleep and circadian function under environmental challenge conditions, and measuring the impact on hypothalamic gene expression and hormonal regulation. We also measure the effects of sleep and wake promoting agents on gene regulation in hypothalamic sleep centers. Because the hypothalamus is important for age-related changes in reproductive function such as puberty and menopause, we are keenly interested in the effects of age and gender on the responses of sleep to environmental challenge. Our goal is to identify the hypothalamic factors that drive sleep and wakefulness and detail the impact of age and gender on hypothalamic sleep regulation.