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The Journal of Neuroscience, July 9, 2008, 28(28):7193-7201; doi:10.1523/JNEUROSCI.1150-08.2008

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Cellular/Molecular
Sleep Deprivation Effects on Circadian Clock Gene Expression in the Cerebral Cortex Parallel Electroencephalographic Differences among Mouse Strains

Jonathan P. Wisor,¹ Ravi K. Pasumarthi,¹ Dmitry Gerashchenko,¹ Carol L. Thompson,² Sayan Pathak,² Aziz Sancar,³ Paul Franken,⁴ Ed S. Lein,² and Thomas S. Kilduff¹

¹Biosciences Division, SRI International, Menlo Park, California 94025, ²Allen Institute for Brain Science, Seattle, Washington 98103, ³Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599, and ⁴Department of Biological Sciences, Stanford University, Stanford, California 94305

Correspondence should be addressed to Dr. Jonathan P. Wisor, Biosciences Division, SRI International, Menlo Park, CA 94025. Email: jonathan.wisor{at}sri.com

Sleep deprivation (SD) results in increased electroencephalographic (EEG) delta power during subsequent non-rapid eye movement sleep (NREMS) and is associated with changes in the expression of circadian clock-related genes in the cerebral cortex. The increase of NREMS delta power as a function of previous wake duration varies among inbred mouse strains. We sought to determine whether SD-dependent changes in circadian clock gene expression parallel this strain difference described previously at the EEG level. The effects of enforced wakefulness of incremental durations of up to 6 h on the expression of circadian clock genes (bmal1, clock, cry1, cry2, csnk1, npas2, per1, and per2) were assessed in AKR/J, C57BL/6J, and DBA/2J mice, three strains that exhibit distinct EEG responses to SD. Cortical expression of clock genes subsequent to SD was proportional to the increase in delta power that occurs in inbred strains: the strain that exhibits the most robust EEG response to SD (AKR/J) exhibited dramatic increases in expression of bmal1, clock, cry2, csnkI, and npas2, whereas the strain with the least robust response to SD (DBA/2) exhibited either no change or a decrease in expression of these genes and cry1. The effect of SD on circadian clock gene expression was maintained in mice in which both of the cryptochrome genes were genetically inactivated. cry1 and cry2 appear to be redundant in sleep regulation as elimination of either of these genes did not result in a significant deficit in sleep homeostasis. These data demonstrate transcriptional regulatory correlates to previously described strain differences at the EEG level and raise the possibility that genetic differences underlying circadian clock gene expression may drive the EEG differences among these strains.

Key words: E-box; delta power; real-time PCR; immediate early genes; mouse strain differences; sleep homeostasis

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Received Jan. 18, 2008; revised May 7, 2008; accepted May 27, 2008.

Correspondence should be addressed to Dr. Jonathan P. Wisor, Biosciences Division, SRI International, Menlo Park, CA 94025. Email: jonathan.wisor{at}sri.com

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