A role for cryptochromesin sleep regulation

Dec 24, 2002BMC neuroscience

Cryptochromes may help regulate sleep

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Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

Mice lacking cryptochrome 1 and 2 genes display high non-REM sleep drive under various conditions.

Cry1,2-/- mice show increased non-REM sleep time, consolidation, and EEG delta power.
Elevated brain mRNA levels of period 1 and 2, and albumin d-binding protein are observed in cry1,2-/- mice.
Period 1 and 2 mRNA levels increase, while albumin d-binding protein mRNA levels decrease in wild type mice and rats after sleep deprivation.
Changes in mRNA levels related to sleep deprivation revert with recovery sleep.
Other circadian gene expressions remain unchanged following sleep deprivation.

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BACKGROUND: The cryptochrome 1 and 2 genes (cry1 and cry2) are necessary for the generation of circadian rhythms, as mice lacking both of these genes (cry1,2-/-) lack circadian rhythms. We studied sleep in cry1,2-/- mice under baseline conditions as well as under conditions of constant darkness and enforced wakefulness to determine whether cryptochromes influence sleep regulatory processes.

RESULTS: Under all three conditions, cry1,2-/- mice exhibit the hallmarks of high non-REM sleep (NREMS) drive (i.e., increases in NREMS time, NREMS consolidation, and EEG delta power during NREMS). This unexpected phenotype was associated with elevated brain mRNA levels of period 1 and 2 (per1,2), and albumin d-binding protein (dbp), which are known to be transcriptionally inhibited by CRY1,2. To further examine the relationship between circadian genes and sleep homeostasis, we examined wild type mice and rats following sleep deprivation and found increased levels of per1,2 mRNA and decreased levels of dbp mRNA specifically in the cerebral cortex; these changes subsided with recovery sleep. The expression of per3, cry1,2, clock, npas2, bmal1, and casein-kinase-1epsilon did not change with sleep deprivation.

CONCLUSIONS: These results indicate that mice lacking cryptochromes are not simply a genetic model of circadian arrhythmicity in rodents and functionally implicate cryptochromes in the homeostatic regulation of sleep.

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A role for cryptochromesin sleep regulation

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