ArticlePloS one2013
Histamine-HisCl1 receptor axis regulates wake-promoting signals in Drosophila melanogaster.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 44 citations in OpenAlex.
- A day sleep promoting role of phototransduction inNeurobiology of sleep and circadian rhythms · 2026Article
- Behavioural phase transitions in the migratory locust,ISME communications · 2026Article
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- A Closer Look at Histamine inInternational journal of molecular sciences · 2024Review
- Drosophila mutants lacking the glial neurotransmitter-modifying enzyme Ebony exhibit low neurotransmitter levels and altered behavior.Scientific reports · 2023Article
- How Temperature Influences Sleep.International journal of molecular sciences · 2022Review
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- Light exposure during development affects physiology of adults inFrontiers in physiology · 2022Article
- Communication Among Photoreceptors and the Central Clock Affects Sleep Profile.Frontiers in physiology · 2020Article
- Better Sleep at Night: How Light Influences Sleep inFrontiers in physiology · 2020Review
- Histidine is selectively required for the growth of Myc-dependent dedifferentiation tumours in theThe EMBO journal · 2019Article
- The neurobiological basis of sleep: Insights from Drosophila.Neuroscience and biobehavioral reviews · 2018Review
- To sleep or not to sleep: neuronal and ecological insights.Current opinion in neurobiology · 2017Review
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- Neuronal substrates for initiation, maintenance, and structural organization of sleep/wake states.F1000Research · 2017Review
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- Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histamine and its two receptors, histamine-gated chloride channel subunit 1 (HisCl1) and ora transientless (Ort), are known to control photoreception and temperature sensing in Drosophila. However, histamine signaling in the context of neural circuitry for sleep-wake behaviors has not yet been examined in detail. Here, we obtained mutant flies with compromised or enhanced histamine signaling and tested their baseline sleep. Hypomorphic mutations in histidine decarboxylase (HDC), an enzyme catalyzing the conversion from histidine to histamine, caused an increase in sleep duration. Interestingly, hisCl1 mutants but not ort mutants showed long-sleep phenotypes similar to those in hdc mutants. Increased sleep duration in hisCl1 mutants was rescued by overexpressing hisCl1 in circadian pacemaker neurons expressing a neuropeptide pigment dispersing factor (PDF). Consistently, RNA interference (RNAi)-mediated depletion of hisCl1 in PDF neurons was sufficient to mimic hisCl1 mutant phenotypes, suggesting that PDF neurons are crucial for sleep regulation by the histamine-HisCl1 signaling. Finally, either hisCl1 mutation or genetic ablation of PDF neurons dampened wake-promoting effects of elevated histamine signaling via direct histamine administration. Taken together, these data clearly demonstrate that the histamine-HisCl1 receptor axis can activate and maintain the wake state in Drosophila and that wake-activating signals may travel via the PDF neurons.
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