Alpha Omega Alpha Honor Medical Society

2010 Research Abstract

Effects of the amplification of the Bmal1 gene expression on the mammalian sleep-wake cycle

Investigator: Constantin Chikando, Morehouse School of Medicine
Mentor: Ketema Nanamdi Paul, PhD, Department of Anatomy and Neurobiology, Morehouse School of Medicine

Sleep deprivation plays a role in a large number of human disorders. Although we understand that sleep is important we still know very little about the cellular and molecular mechanisms that govern it. While there is a wide body of research focused on the issues of hyperarousal and circadian dysregulation there are relatively few investigations that explore how homeostatic dysregulation is related to the onset of insomnia. This study describes the influence of the Bmal1gene on sleep and wakefulness in mice, the primary mammalian genetic model for sleep analysis, and tests the hypothesis that over-expression of this gene component will increase wake amount and enhance the homeostatic response to extended wakefulness.

Electroencephalogram/electromyogram sleep-wake patterns were recorded in wildtype and transgenic C57Bl/6J mice maintained on a 12-hour light: 12-hour dark schedule. Following a 24- hour baseline recording, mice were sleep deprived during the first 6 hours of the light phase by gentle handling and then given an 18-hour recovery opportunity. Bmal1 overexpression mice and littermate controls exhibited no differences in sleep and wakefulness during 24 hours of baseline recording. Though the recovery response of REM sleep was similar between transgenic mice and control, when examined in reference to baseline levels, transgenic mice exhibited a less robust recovery response in NREM sleep. These results suggest that enhancing Bmal1 expression exclusively in skeletal muscle tissue impairs the ability to recover from sleep deprivation.

Updated on January 6, 2011.

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