Altered Sleep Homeostasis in Knockout Mice
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چکیده
INTRODUCTION The timing and quality of sleep are controlled by the interaction of a homeostatic process, that tracks sleep need as a function of the previous sleep/wake history, and a circadian process that ensures the appropriate timing of sleep relative to the daily light-dark alternation.1,2 Although these two processes seem functionally and neurophysiologically distinct, at the molecular level, several core components of the circadian timing system were found to also play a role in maintaining proper sleep homeostasis.3,4 The molecular circadian oscillator consists of positive and negative elements. In mammals the positive elements comprise of CLOCK, NPAS2, and BMAL1, with CLOCK/ NPAS2:BMAL1 heterodimers driving the transcription of many target genes including that of the Period (Per1, -2) and Cryptochrome (Cry1, -2 ) genes.5 PER:CRY protein complexes suppress CLOCK/NPAS2:BMAL1-mediated transcription, including their own, thereby constituting the negative elements in this core feedback loop. Additional interactions between these core clock genes at the level of transcription, transloca-
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تاریخ انتشار 2016