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- W2316549597 abstract "Introduction Increasing evidence suggests that clock genes may be implicated in a spectrum of psychiatric diseases, including sleep and mood related disorders as well as schizophrenia. The bHLH transcription factors SHARP1/DEC2/BHLHE41 and SHARP2/DEC1/BHLHE40 are modulators of the circadian system and SHARP1/DEC2/BHLHE40 has been shown to regulate homeostatic sleep drive in humans. Methods In this study, we characterized Sharp1 and Sharp2 double mutant mice (S1/2-/-) using online EEG recordings in living animals, behavioral assays, global gene expression profiling and bioinformatic modeling. Gene expression in human brains samples was performed with qRT-PCR. Results EEG recordings revealed attenuated sleep/wake amplitudes and alterations of theta oscillations. Increased sleep in the dark phase is paralleled by reduced voluntary activity and cortical gene expression signatures reveal associations with psychiatric diseases. S1/2-/- mice display alterations in novelty induced activity, anxiety and curiosity. Moreover, mutant mice exhibit impaired working memory and deficits in prepulse inhibition resembling symptoms of psychiatric diseases. Network modeling indicates a connection between neural plasticity and clock genes, particularly for SHARP1 and PER1 , which are also significantly downregulated in the frontal cortex of schizophrenic patients. Conclusions Our findings support the hypothesis that abnormal sleep and certain (endo)phenotypes of psychiatric diseases may be caused by common mechanisms involving components of the molecular clock including SHARP1 and SHARP2" @default.
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- W2316549597 date "2014-01-01" @default.
- W2316549597 modified "2023-09-27" @default.
- W2316549597 title "EPA-0692 – Mice lacking the circadian modulators sharp1 and sharp2 display altered sleep and mixed state endophenotypes of psychiatric disorders" @default.
- W2316549597 doi "https://doi.org/10.1016/s0924-9338(14)78057-5" @default.
- W2316549597 hasPublicationYear "2014" @default.
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