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• W2116701778 startingPage "e68269" @default.
• W2116701778 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." @default.
• W2116701778 created "2016-06-24" @default.
• W2116701778 creator A5038019104 @default.
• W2116701778 creator A5042501304 @default.
• W2116701778 creator A5070944340 @default.
• W2116701778 creator A5083816637 @default.
• W2116701778 date "2013-07-03" @default.
• W2116701778 modified "2023-10-03" @default.
• W2116701778 title "Histamine-HisCl1 Receptor Axis Regulates Wake-Promoting Signals in Drosophila melanogaster" @default.
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• W2116701778 doi "https://doi.org/10.1371/journal.pone.0068269" @default.
• W2116701778 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3700972" @default.
• W2116701778 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23844178" @default.
• W2116701778 hasPublicationYear "2013" @default.
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• W2116701778 hasAuthorship W2116701778A5070944340 @default.
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