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      Circadian Rhythms in the Neuronal Network Timing the Luteinizing Hormone Surge

      1 , 1 , 2
      Endocrinology
      The Endocrine Society

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          Abstract

          For billions of years before electric light was invented, life on Earth evolved under the pattern of light during the day and darkness during the night. Through evolution, nearly all organisms internalized the temporal rhythm of Earth’s 24-hour rotation and evolved self-sustaining biological clocks with a ~24-hour rhythm. These internal rhythms are called circadian rhythms, and the molecular constituents that generate them are called molecular circadian clocks. Alignment of molecular clocks with the environmental light-dark rhythms optimizes physiology and behavior. This phenomenon is particularly true for reproductive function, in which seasonal breeders use day length information to time yearly changes in fertility. However, it is becoming increasingly clear that light-induced disruption of circadian rhythms can negatively impact fertility in nonseasonal breeders as well. In particular, the luteinizing hormone surge promoting ovulation is sensitive to circadian disruption. In this review, we will summarize our current understanding of the neuronal networks that underlie circadian rhythms and the luteinizing hormone surge.

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          Most cited references105

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          Circadian clock genes and the transcriptional architecture of the clock mechanism

          The mammalian circadian clock has evolved as an adaptation to the 24-h light/darkness cycle on earth. Maintaining cellular activities in synchrony with the activities of the organism (such as eating and sleeping) helps different tissue and organ systems coordinate and optimize their performance. The full extent of the mechanisms by which cells maintain the clock are still under investigation, but involve a core set of clock genes that regulate large networks of gene transcription both by direct transcriptional activation/repression as well as the recruitment of proteins that modify chromatin states more broadly.
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            Timing of expression of the core clock gene Bmal1 influences its effects on aging and survival.

            The absence of Bmal1, a core clock gene, results in a loss of circadian rhythms, an acceleration of aging, and a shortened life span in mice. To address the importance of circadian rhythms in the aging process, we generated conditional Bmal1 knockout mice that lacked the BMAL1 protein during adult life and found that wild-type circadian variations in wheel-running activity, heart rate, and blood pressure were abolished. Ocular abnormalities and brain astrogliosis were conserved irrespective of the timing of Bmal1 deletion. However, life span, fertility, body weight, blood glucose levels, and age-dependent arthropathy, which are altered in standard Bmal1 knockout mice, remained unaltered, whereas atherosclerosis and hair growth improved, in the conditional adult-life Bmal1 knockout mice, despite abolition of clock function. Hepatic RNA-Seq revealed that expression of oscillatory genes was dampened in the adult-life Bmal1 knockout mice, whereas overall gene expression was largely unchanged. Thus, many phenotypes in conventional Bmal1 knockout mice, hitherto attributed to disruption of circadian rhythms, reflect the loss of properties of BMAL1 that are independent of its role in the clock. These findings prompt reevaluation of the systemic consequences of disruption of the molecular clock.
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              Spatiotemporal single-cell analysis of gene expression in the mouse suprachiasmatic nucleus

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                Author and article information

                Contributors
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                Journal
                Endocrinology
                The Endocrine Society
                0013-7227
                1945-7170
                February 01 2022
                February 01 2022
                February 01 2022
                February 01 2022
                December 30 2021
                : 163
                : 2
                Affiliations
                [1 ]Department of Obstetrics, Gynecology, and Reproductive Sciences, Center for Reproductive Science and Medicine, University of California, San Diego, La Jolla, CA, 92093, USA
                [2 ]Department of Animal Science and the Reproductive and Developmental Sciences Program, Michigan State University, 766 Service Road, East Lansing, MI, 48824, USA
                Article
                10.1210/endocr/bqab268
                34967900
                b45bd91f-91ce-4d58-9f16-22b3a9b05b06
                © 2021

                https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model

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