ArticleJournal of neurophysiology2015
5-HT2A receptor activation is necessary for CO2-induced arousal.
Article in Journal of neurophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 67 citations in OpenAlex.
- Effect of Pimavanserin on the Respiratory Arousal Threshold from Sleep: A Randomized Trial.Annals of the American Thoracic Society · 2022Trial
- Leptin alleviates obesity hypoventilationbioRxiv : the preprint server for biology · 2026Article
- Serotonin Associated Mechanisms in Sudden Unexpected Death in Epilepsy: A Review.Revista de neurologia · 2026Review
- Altered Interictal Bed Nucleus of Stria Terminalis Connectivity in Patients With Temporal Lobe Epilepsy.Neurology · 2025Article
- Altered PI3K/mTOR Signaling within the Forebrain Leads to Respiratory Deficits in a Mouse Model of Epilepsy.eNeuro · 2025Article
- Respiratory and Metabolic Effects of Active Expiration in Freely Behaving Rats.Acta physiologica (Oxford, England) · 2025Article
- MK-212 precipitates seizure-induced death in amygdala-kindled mice via a non-5-HTEpilepsy & behavior : E&B · 2025Article
- Sudden unexpected death in epilepsy: respiratory vs. cardiac contributions.Cardiovascular research · 2025Review
- Sudden Unexpected Death in Epilepsy: Central Respiratory Chemoreception.International journal of molecular sciences · 2025Review
- Author response to Panza et al.The Journal of physiology · 2025Article
- Psychotomimetic compensation versus sensitization.Pharmacology research & perspectives · 2024Review
- Altered 5-HT2A/C receptor binding in the medulla oblongata in the sudden infant death syndrome (SIDS): Part II. Age-associated alterations in serotonin receptor binding profiles within medullary nuclei supporting cardiorespiratory homeostasis.Journal of neuropathology and experimental neurology · 2024Article
- Altered 5-HT2A/C receptor binding in the medulla oblongata in the sudden infant death syndrome (SIDS): Part I. Tissue-based evidence for serotonin receptor signaling abnormalities in cardiorespiratory- and arousal-related circuits.Journal of neuropathology and experimental neurology · 2023Article
- The fundamental need for unifying phenotypes in sudden unexpected pediatric deaths.Frontiers in medicine · 2023Article
- Serotonin receptors in epilepsy: Novel treatment targets?Epilepsia open · 2022Review
- Central respiratory chemoreception.Handbook of clinical neurology · 2022Review
- The role of sleep state and time of day in modulating breathing in epilepsy: implications for sudden unexpected death in epilepsy.Frontiers in neural circuits · 2022Review
- Use of Zebrafish Models to Boost Research in Rare Genetic Diseases.International journal of molecular sciences · 2021Review
- Locus Coeruleus Acid-Sensing Ion Channels Modulate Sleep-Wakefulness and State Transition from NREM to REM Sleep in the Rat.Neuroscience bulletin · 2021Article
- Chemoreceptor mechanisms regulating COThe Journal of physiology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Hypercapnia-induced arousal from sleep is an important protective mechanism pertinent to a number of diseases. Most notably among these are the sudden infant death syndrome, obstructive sleep apnea and sudden unexpected death in epilepsy. Serotonin (5-HT) plays a significant role in hypercapnia-induced arousal. The mechanism of 5-HT's role in this protective response is unknown. Here we sought to identify the specific 5-HT receptor subtype(s) involved in this response. Wild-type mice were pretreated with antagonists against 5-HT receptor subtypes, as well as antagonists against adrenergic, cholinergic, histaminergic, dopaminergic, and orexinergic receptors before challenge with inspired CO2 or hypoxia. Antagonists of 5-HT(2A) receptors dose-dependently blocked CO2-induced arousal. The 5-HT(2C) receptor antagonist, RS-102221, and the 5-HT1A receptor agonist, 8-OH-DPAT, attenuated but did not completely block CO2-induced arousal. Blockade of non-5-HT receptors did not affect CO2-induced arousal. None of these drugs had any effect on hypoxia-induced arousal. 5-HT2 receptor agonists were given to mice in which 5-HT neurons had been genetically eliminated during embryonic life (Lmx1b(f/f/p)) and which are known to lack CO2-induced arousal. Application of agonists to 5-HT(2A), but not 5-HT(2C), receptors, dose-dependently restored CO2-induced arousal in these mice. These data identify the 5-HT(2A) receptor as an important mediator of CO2-induced arousal and suggest that, while 5-HT neurons can be independently activated to drive CO2-induced arousal, in the absence of 5-HT neurons and endogenous 5-HT, 5-HT receptor activation can act in a permissive fashion to facilitate CO2-induced arousal via another as yet unidentified chemosensor system.
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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.