ArticleCerebral cortex (New York, N.Y. : 1991)2019
Excitation of Cortical nNOS/NK1R Neurons by Hypocretin 1 is Independent of Sleep Homeostasis.
Article in Cerebral cortex (New York, N.Y. : 1991), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- Type-I nNOS neurons orchestrate cortical neural activity and vasomotion.bioRxiv : the preprint server for biology · 2025Article
- Mediation Effect of CSF Substance P on the Association Between Smoking and Sleep.Brain and behavior · 2025Article
- Long-range inhibitory neurons mediate cortical neurovascular coupling.Cell reports · 2024Article
- Parvalbumin interneuron activity drives fast inhibition-induced vasoconstriction followed by slow substance P-mediated vasodilation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Declining Levels of Specialized Synaptic Surface Proteins in nNOS-Expressing Interneurons in Mice Treated Prenatally with Valproic Acid.Neurochemical research · 2021Article
- Article
- Experience and sleep-dependent synaptic plasticity: from structure to activity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Review
- Hypocretin as a Hub for Arousal and Motivation.Frontiers in neurology · 2018Review
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
Abstract
We have proposed that cortical nNOS/NK1R interneurons have a role in sleep homeostasis. The hypocretins (orexins) are wake-promoting neuropeptides and hypocretin/orexin (Hcrt) neurons project to the cortex. Hcrt peptides affect deep layer cortical neurons, and Hcrt receptor 1 (Hcrtr1; Ox1r) mRNA is expressed in cortical nNOS/NK1R cells. Therefore, we investigated whether Hcrt neuron stimulation affects cingulate cortex nNOS/NK1R neurons. Bath application of HCRT1/orexin-A evoked an inward current and membrane depolarization in most nNOS/NK1R cells which persisted in tetrodotoxin; optogenetic stimulation of Hcrt terminals expressing channelrhodopsin-2 confirmed these results, and pharmacological studies determined that HCRTR1 mediated these responses. Single-cell RT-PCR found Hcrtr1 mRNA in 31% of nNOS/NK1R cells without any Hcrtr2 mRNA expression; immunohistochemical studies of Hcrtr1-EGFP mice confirmed that a minority of nNOS/NK1R cells express HCRTR1. When Hcrt neurons degenerated in orexin-tTA;TetO DTA mice, the increased EEG delta power during NREM sleep produced in response to 4 h sleep deprivation and c-FOS expression in cortical nNOS/NK1R cells during recovery sleep were indistinguishable from that of controls. We conclude that Hcrt excitatory input to these deep layer cells is mediated through HCRTR1 but is unlikely to be involved in the putative role of cortical nNOS/NK1R neurons in sleep homeostasis.
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