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Background  We have previously reported that the expression of circadian clock-genes increases in the cerebral cortex after sleep deprivation (SD) and that the sleep rebound following SD is attenuated in mice deficient for one or more clock-genes. We hypothesized that besides generating circadian rhythms, clock-genes also play a role in the homeostatic regulation of sleep. Here we follow the time course of the forebrain changes in the expression of the clock-genes  period  ( per )- 1, per2 , and of the clock-controlled gene  albumin D-binding protein  ( dbp ) during a 6 h SD and subsequent recovery sleep in three inbred strains of mice for which the homeostatic sleep rebound following SD differs. We reasoned that if clock genes are functionally implicated in sleep homeostasis then the SD-induced changes in gene expression should vary according to the genotypic differences in the sleep rebound.    Results  In all three strains  per  expression was increased when animals were kept awake but the rate of increase during the SD as well as the relative increase in  per  after 6 h SD were highest in the strain for which the sleep rebound was smallest; i.e., DBA/2J (D2). Moreover, whereas in the other two strains  per1  and  per2  reverted to control levels with recovery sleep,  per2  expression specifically, remained elevated in D2 mice.  dbp  expression increased during the light period both during baseline and during SD although levels were reduced during the latter condition compared to baseline. In contrast to  per2 ,  dbp  expression reverted to control levels with recovery sleep in D2 only, whereas in the two other strains expression remained decreased.    Conclusion  These findings support and extend our previous findings that clock genes in the forebrain are implicated in the homeostatic regulation of sleep and suggest that sustained, high levels of  per2  expression may negatively impact recovery sleep.

A non-circadian role for clock-genes in sleep homeostasis:a strain comparison