Abstract
Circadian rhythms are related to various psychiatric disorders. Recently, antipsychotics, including quetiapine (QTP), have been accepted as potential therapeutic agents for the treatment of depression, but its mechanism remains poorly understood. In this study, we examined clock gene fluctuation patterns in QTP-treated mice. QTP significantly increased Per2 mRNA at ZT12 and Per1 and Per2 expression at ZT18 in the amygdala. There were significant differences between the control and QTP groups in the cross-time effects of Per2 mRNA expression in the amygdala. Our findings suggest that QTP possibly acts on the circadian system, which then induces changes in mood symptoms.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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ARNTL Transcription Factors / genetics
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ARNTL Transcription Factors / metabolism*
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Amygdala / metabolism*
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Animals
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Antipsychotic Agents / pharmacology*
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Antipsychotic Agents / therapeutic use
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Biological Clocks / genetics
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Biological Clocks / physiology
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Depression / drug therapy
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Depression / etiology
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Depression / genetics
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Dibenzothiazepines / pharmacology*
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Dibenzothiazepines / therapeutic use
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Gene Expression Regulation / drug effects*
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Hippocampus / metabolism*
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Male
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Mice, Inbred C57BL
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Molecular Targeted Therapy
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Period Circadian Proteins / genetics
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Period Circadian Proteins / metabolism*
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Quetiapine Fumarate
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RNA, Messenger / metabolism
Substances
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ARNTL Transcription Factors
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Antipsychotic Agents
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Bmal1 protein, mouse
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Dibenzothiazepines
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Per1 protein, mouse
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Per2 protein, mouse
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Period Circadian Proteins
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RNA, Messenger
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Quetiapine Fumarate