ReviewRespiratory physiology & neurobiology2009
Medullary serotonin defects and respiratory dysfunction in sudden infant death syndrome.
Review in Respiratory physiology & neurobiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 60 citations in OpenAlex.
- Obstructive Sleep Apnea and Serotoninergic Signalling Pathway: Pathomechanism and Therapeutic Potential.International journal of molecular sciences · 2024Review
- 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
- Nicotine on the developing brain.Pharmacological research · 2023Review
- Influence of developmental nicotine exposure on serotonergic control of breathing-related motor output.Developmental neurobiology · 2022Article
- Nicotinic Receptors in the Brainstem Ascending Arousal System in SIDS With Analysis of Pre-natal Exposures to Maternal Smoking and Alcohol in High-Risk Populations of the Safe Passage Study.Frontiers in neurology · 2021Article
- Hypertrophy of the Anterior External Arcuate Fasciculus: A Rare Variant With Implications for the Development of the Arcuate Nucleus.Frontiers in neuroanatomy · 2020Article
- Article
- Microglia modulate brainstem serotonergic expression following neonatal sustained hypoxia exposure: implications for sudden infant death syndrome.The Journal of physiology · 2016Article
- Polymorphisms in genes of respiratory control and sudden infant death syndrome.International journal of legal medicine · 2015Article
- Sudden unexpected death in epilepsy: addressing the challenges.Current neurology and neuroscience reports · 2014Review
- Loss of motoneurons in the ventral compartment of the rat hypoglossal nucleus following early postnatal exposure to alcohol.Journal of chemical neuroanatomy · 2013Article
- Dynamics of neuromodulatory feedback determines frequency modulation in a reduced respiratory network: a computational study.Respiratory physiology & neurobiology · 2013Article
- Gestational stress promotes pathological apneas and sex-specific disruption of respiratory control development in newborn rat.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Understanding the rhythm of breathing: so near, yet so far.Annual review of physiology · 2013Review
- Pontine mechanisms of respiratory control.Comprehensive Physiology · 2012Review
- Cardiac ion channelopathies and the sudden infant death syndrome.ISRN cardiology · 2012Article
- 5HT1A receptors inhibit glutamate inputs to cardiac vagal neurons post-hypoxia/hypercapnia.Respiratory physiology & neurobiology · 2011Article
- Gene variants predisposing to SIDS: current knowledge.Forensic science, medicine, and pathology · 2011Review
- Chapter 3--networks within networks: the neuronal control of breathing.Progress in brain research · 2011Review
- The role of serotonin in respiratory function and dysfunction.Respiratory physiology & neurobiology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Sudden infant death syndrome (SIDS) is defined as the sudden and unexpected death of an infant less than 12 months of age that occurs during sleep and remains unexplained after a complete autopsy, death scene investigation, and review of the clinical history. It is the leading cause of postneonatal mortality in the developed world. The cause of SIDS is unknown, but is postulated to involve impairment of brainstem-mediated homeostatic control. Extensive evidence from animal studies indicates that serotonin (5-HT) neurons in the medulla oblongata play a role in the regulation of multiple aspects of respiratory and autonomic function. A subset of SIDS infants have several abnormalities in medullary markers of 5-HT function and genetic polymorphisms impacting the 5-HT system, informing the hypothesis that SIDS results from a defect in 5-HT brainstem-mediated control of respiratory (and autonomic) regulation. Here we review the evidence from postmortem human studies and animal studies to support this hypothesis and discuss how the pathogenesis of SIDS is likely to originate in utero during fetal development.
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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.