2008 Eighth Annual Beckman Scholars Symposium
Saturday Poster Session - July 29, 2006

Circadian rhythms (driven by biological 24-hour internal clocks entrained by the light-dark cycle) and sleep homeostatic mechanisms (an organism's increasing sleep-drive with increasing sleep deprivation) both determine an organism's level of sleepiness. The suprachiasmatic nucleus (SCN), a cluster of about 10,000 cells within the hypothalamus above the optic chiasm, houses mammals' master circadian pacemaker. In mice, the SCN is known to oscillate in accordance with the expression of a small number of "clock-genes": period genes per1 and per2 (per1,2); cryptochrome genes cry1 and cry2 (cry1,2); and transcriptional regulators clock and bmal1. Recent data on mice lacking cry1,2 and per1,2 indicates that clock-genes have a key role in sleep homeostasis as well that most likely involves their expression outside the SCN. Upon investigating changes in the expression of these genes following increasing periods of sleep deprivation and recovery sleep, we find that per1,2 mRNAs tend to increase in the forebrain with increasing amounts of wakefulness. This was investigated in two different strains of mice that differ in various sleep parameters. In addition to changes in the forebrain, we are now investigating these changes in the cerebellum (a brain region long ignored in sleep physiology), but which is increasingly thought to play a variety of roles, including sleep/wake behaviors.