ArticlePloS one2014
Pet-1 deficiency alters the circadian clock and its temporal organization of behavior.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Circadian NAD(P)(H) cycles in cell metabolism.Seminars in cell & developmental biology · 2022Review
- Article
- Rhythms, Reward, and Blues: Consequences of Circadian Photoperiod on Affective and Reward Circuit Function.Neuroscience · 2021Review
- Distinct Components of Photoperiodic Light Are Differentially Encoded by the Mammalian Circadian Clock.Journal of biological rhythms · 2020Article
- Potential Pathways for Circadian Dysfunction and Sundowning-Related Behavioral Aggression in Alzheimer's Disease and Related Dementias.Frontiers in neuroscience · 2020Review
- The ETS-5 transcription factor regulates activity states inProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Adult Brain Serotonin Deficiency Causes Hyperactivity, Circadian Disruption, and Elimination of Siestas.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Abnormal cell-intrinsic and network excitability in the neocortex of serotonin-deficient Pet-1 knockout mice.Journal of neurophysiology · 2016Article
- The sleep-wake cycle and motor activity, but not temperature, are disrupted over the light-dark cycle in mice genetically depleted of serotonin.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The serotonin and circadian systems are two important interactive regulatory networks in the mammalian brain that regulate behavior and physiology in ways that are known to impact human mental health. Previous work on the interaction between these two systems suggests that serotonin modulates photic input to the central circadian clock (the suprachiasmatic nuclei; SCN) from the retina and serves as a signal for locomotor activity, novelty, and arousal to shift the SCN clock, but effects of disruption of serotonergic signaling from the raphe nuclei on circadian behavior and on SCN function are not fully characterized. In this study, we examined the effects on diurnal and circadian behavior, and on ex vivo molecular rhythms of the SCN, of genetic deficiency in Pet-1, an ETS transcription factor that is necessary to establish and maintain the serotonergic phenotype of raphe neurons. Pet-1⁻/⁻ mice exhibit loss of rhythmic behavioral coherence and an extended daily activity duration, as well as changes in the molecular rhythms expressed by the clock, such that ex vivo SCN from Pet-1⁻/⁻ mice exhibit period lengthening and sex-dependent changes in rhythmic amplitude. Together, our results indicate that Pet-1 regulation of raphe neuron serotonin phenotype contributes to the period, precision and light/dark partitioning of locomotor behavioral rhythms by the circadian clock through direct actions on the SCN clock itself, as well as through non-clock effects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.