ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Bmal1 is an essential regulator for circadian cytosolic Ca²⁺ rhythms in suprachiasmatic nucleus neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 42 citations in OpenAlex.
- The intersection of circadian rhythms and the blood-brain barrier with drug efficacy and delivery in neurological disorders.Advanced drug delivery reviews · 2025Review
- Hepatocellular Carcinoma in Mice Affects Neuronal Activity and Glia Cells in the Suprachiasmatic Nucleus.Biomedicines · 2024Article
- The Suprachiasmatic Nucleus at 50: Looking Back, Then Looking Forward.Journal of biological rhythms · 2024Review
- Circadian Rhythms of the Blood-Brain Barrier and Drug Delivery.Circulation research · 2024Review
- Cold-induced suspension and resetting of CaiScience · 2023Article
- In vivo recording of the circadian calcium rhythm in Prokineticin 2 neurons of the suprachiasmatic nucleus.Scientific reports · 2023Article
- Network-driven intracellular cAMP coordinates circadian rhythm in the suprachiasmatic nucleus.Science advances · 2023Article
- In-phasic cytosolic-nuclear CaFrontiers in neuroscience · 2023Article
- Comparative CaBiophysical reports · 2021Article
- Sleep/wake calcium dynamics, respiratory function, and ROS production in cardiac mitochondria.Journal of advanced research · 2021Article
- Cellular clocks in hyperoxia effects on [CaAmerican journal of physiology. Lung cellular and molecular physiology · 2021Article
- Reciprocal Relationship Between Calcium Signaling and Circadian Clocks: Implications for Calcium Homeostasis, Clock Function, and Therapeutics.Frontiers in molecular neuroscience · 2021Review
- Cisplatin's dual-effect on the circadian clock triggers proliferation and apoptosis.Neurobiology of sleep and circadian rhythms · 2020Review
- Ion Channels Controlling Circadian Rhythms in Suprachiasmatic Nucleus Excitability.Physiological reviews · 2020Review
- Bringing the cellular clock into understanding lung disease: it's time, period!American journal of physiology. Lung cellular and molecular physiology · 2020Article
- It's about time: clocks in the developing lung.The Journal of clinical investigation · 2020Review
- NSP-C contributes to the upregulation of CLOCK/BMAL1-mediated transcription.Cytotechnology · 2019Article
- GABA in the suprachiasmatic nucleus refines circadian output rhythms in mice.Communications biology · 2019Article
- Differential contribution of CaThe Journal of general physiology · 2018Article
- Rhythms of metabolism in adipose tissue and mitochondria.Neurobiology of sleep and circadian rhythms · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hypothalamic suprachiasmatic nucleus (SCN) plays a pivotal role in the mammalian circadian clock system. Bmal1 is a clock gene that drives transcriptional-translational feedback loops (TTFLs) for itself and other genes, and is expressed in nearly all SCN neurons. Despite strong evidence that Bmal1-null mutant mice display arrhythmic behavior under constant darkness, the function of Bmal1 in neuronal activity is unknown. Recently, periodic changes in the levels of intracellular signaling messengers, such as cytosolic Ca(2+) and cAMP, were suggested to regulate TTFLs. However, the opposite aspect of how clock gene TTFLs regulate cytosolic signaling remains unclear. To investigate intracellular Ca(2+) dynamics under Bmal1 perturbations, we cotransfected some SCN neurons with yellow cameleon together with wild-type or dominant-negative Bmal1 using a gene-gun applied for mouse organotypic cultures. Immunofluorescence staining for a tag protein linked to BMAL1 showed nuclear expression of wild-type BMAL1 and its degradation within 1 week after transfection in SCN neurons. However, dominant-negative BMAL1 did not translocate into the nucleus and the cytosolic signals persisted beyond 1 week. Consistently, circadian Ca(2+) rhythms in SCN neurons were inhibited for longer periods by dominant-negative Bmal1 overexpression. Furthermore, SCN neurons transfected with a Bmal1 shRNA lengthened, whereas those overexpressing wild-type Bmal1 shortened, the periods of Ca(2+) rhythms, with a significant reduction in their amplitude. BMAL1 expression was intact in the majority of neighboring neurons in organotypic cultures. Therefore, we conclude that proper intrinsic Bmal1 expression, but not passive signaling via cell-to-cell interactions, is the determinant of circadian Ca(2+) rhythms in SCN neurons.
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