Journal article
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, Vol.83(3), pp.144-160
03/2024
DOI: 10.1093/jnen/nlae004
PMCID: PMC10880067
PMID: 38323418
Abstract
The failure of chemoreflexes, arousal, and/or autoresuscitation to asphyxia may underlie some sudden infant death syndrome (SIDS) cases. In Part I, we showed that some SIDS infants had altered 5-hydroxytryptamine (5-HT)2A/C receptor binding in medullary nuclei supporting chemoreflexes, arousal, and autoresuscitation. Here, using the same dataset, we tested the hypotheses that the prevalence of low 5-HT1A and/or 5-HT2A/C receptor binding (defined as levels below the 95% confidence interval of controls-a new approach), and the percentages of nuclei affected are greater in SIDS versus controls, and that the distribution of low binding varied with age of death. The prevalence and percentage of nuclei with low 5-HT1A and 5-HT2A/C binding in SIDS were twice that of controls. The percentage of nuclei with low 5-HT2A/C binding was greater in older SIDS infants. In >80% of older SIDS infants, low 5-HT2A/C binding characterized the hypoglossal nucleus, vagal dorsal nucleus, nucleus of solitary tract, and nuclei of the olivocerebellar subnetwork (important for blood pressure regulation). Together, our findings from SIDS infants and from animal models of serotonergic dysfunction suggest that some SIDS cases represent a serotonopathy. We present new hypotheses, yet to be tested, about how defects within serotonergic subnetworks may lead to SIDS.
Details
- Title: Subtitle
- 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
- Creators
- Kevin J Cummings - University of MissouriJames C Leiter - Dartmouth CollegeFelicia L Trachtenberg - Clinical Research, Carelon Research, Newton, Massachusetts, USABenjamin W Okaty - Harvard UniversityRobert A Darnall - Dartmouth CollegeElisabeth A Haas - Rady Children's Hospital-San DiegoRonald M Harper - David Geffen School of Medicine at UCLAEugene E Nattie - Dartmouth CollegeHenry F Krous - University of California San DiegoOthon J Mena - Dade County Medical Examiner DepartmentGeorge B Richerson - University of IowaSusan M Dymecki - Harvard UniversityHannah C Kinney - Harvard UniversityRobin L Haynes - Harvard University
- Resource Type
- Journal article
- Publication Details
- Journal of neuropathology and experimental neurology, Vol.83(3), pp.144-160
- DOI
- 10.1093/jnen/nlae004
- PMID
- 38323418
- PMCID
- PMC10880067
- NLM abbreviation
- J Neuropathol Exp Neurol
- eISSN
- 1554-6578
- Grant note
- Jacob Neil Boger Foundation for SIDS CJ Murphy Foundation for Solving the Puzzle of SIDS Margot Elizabeth Koslosky Memorial Fund Cooper Trewin Brighter Days Fund River's Gift National Institute of Child Health and Development Robert's Program on Sudden Unexpected Death in Pediatrics Florida SIDS Alliance Jude Theodore Zayac Fund CJ Foundation for SIDS Three Butterflies Foundation First Candle Barrett Tallman Memorial Fund American SIDS Institute
- Language
- English
- Electronic publication date
- 02/07/2024
- Date published
- 03/2024
- Academic Unit
- Neurology; Molecular Physiology and Biophysics; Iowa Neuroscience Institute; Neurosurgery
- Record Identifier
- 9984557942502771
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