ArticleNature communications2020
TRESK is a key regulator of nocturnal suprachiasmatic nucleus dynamics and light adaptive responses.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Evaluation of Novel Cloxyquin Analogs for KArchiv der Pharmazie · 2026Article
- Dissociation between subjective sleep quality and lipid dysregulation in underground miners: night shift work as an independent risk factor for hypercholesterolemia.Frontiers in public health · 2026Article
- Calcium-dependent activation of TREK-1 and TREK-2 background potassium channels by calcineurin.Scientific reports · 2025Article
- The Ubiquitin Ligase Adaptor NDFIP1 Interacts with TRESK and Negatively Regulates the Background KInternational journal of molecular sciences · 2024Article
- Sirenian genomes illuminate the evolution of fully aquatic species within the mammalian superorder afrotheria.Nature communications · 2024Article
- Cloxyquin activates hTRESK by allosteric modulation of the selectivity filter.Communications biology · 2023Article
- Berberine Ameliorates Metabolic-Associated Fatty Liver Disease Mediated Metabolism Disorder and Redox Homeostasis by Upregulating Clock Genes: Clock and Bmal1 Expressions.Molecules (Basel, Switzerland) · 2023Article
- A non-canonical retina-ipRGCs-SCN-PVT visual pathway for mediating contagious itch behavior.Cell reports · 2022Article
- Contribution of Neuronal and Glial Two-Pore-Domain Potassium Channels in Health and Neurological Disorders.Neural plasticity · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The suprachiasmatic nucleus (SCN) is a complex structure dependent upon multiple mechanisms to ensure rhythmic electrical activity that varies between day and night, to determine circadian adaptation and behaviours. SCN neurons are exposed to glutamate from multiple sources including from the retino-hypothalamic tract and from astrocytes. However, the mechanism preventing inappropriate post-synaptic glutamatergic effects is unexplored and unknown. Unexpectedly we discovered that TRESK, a calcium regulated two-pore potassium channel, plays a crucial role in this system. We propose that glutamate activates TRESK through NMDA and AMPA mediated calcium influx and calcineurin activation to then oppose further membrane depolarisation and rising intracellular calcium. Hence, in the absence of TRESK, glutamatergic activity is unregulated leading to membrane depolarisation, increased nocturnal SCN firing, inverted basal calcium levels and impaired sensitivity in light induced phase delays. Our data reveals TRESK plays an essential part in SCN regulatory mechanisms and light induced adaptive behaviours.
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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.