ArticleThe Journal of physiology2016
Microglia modulate brainstem serotonergic expression following neonatal sustained hypoxia exposure: implications for sudden infant death syndrome.
Article in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Neonatal inflammation induces lasting sex- and region-dependent microglia activation and sex-dependent impairments in chemoreflexes.Journal of applied physiology (Bethesda, Md. : 1985) · 2026Article
- Unique infrared thermographic profiles and altered hypothalamic neurochemistry associated with mortality in endotoxic shock.Experimental neurology · 2025Article
- Inflammation in sudden infant death syndrome.Pediatric research · 2024Article
- Cardiorespiratory anomalies and increased brainstem microglia in a rat model of neonatal opioid withdrawal syndrome.Respiratory physiology & neurobiology · 2022Article
- Postnatal Exposure to Brief Hypoxia Alters Brain VEGF Expression and Capillary Density in Adult Mice.Advances in experimental medicine and biology · 2022Article
- Apnea of prematurity and sudden infant death syndrome.Handbook of clinical neurology · 2022Review
- Perinatal Hypoxemia and Oxygen Sensing.Comprehensive Physiology · 2021Article
- Caffeine prevents prostaglandin EAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Peripheral-to-central immune communication at the area postrema glial-barrier following bleomycin-induced sterile lung injury in adult rats.Brain, behavior, and immunity · 2020Article
- Ventilatory and carotid body responses to acute hypoxia in rats exposed to chronic hypoxia during the first and second postnatal weeks.Respiratory physiology & neurobiology · 2020Article
- Impact of inflammation on developing respiratory control networks: rhythm generation, chemoreception and plasticity.Respiratory physiology & neurobiology · 2020Review
- Mechanistic actions of oxygen and methylxanthines on respiratory neural control and for the treatment of neonatal apnea.Respiratory physiology & neurobiology · 2020Review
- Mechanisms underlying a critical period of respiratory development in the rat.Respiratory physiology & neurobiology · 2019Review
- Central and peripheral chemoreceptors in sudden infant death syndrome.The Journal of physiology · 2018Review
- Respiratory dysfunction following neonatal sustained hypoxia exposure during a critical window of brain stem extracellular matrix formation.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Minocycline blocks glial cell activation and ventilatory acclimatization to hypoxia.Journal of neurophysiology · 2017Article
- The impact of inflammation on respiratory plasticity.Experimental neurology · 2017Review
- SIDS-CDF hypothesis revisited: explaining hypoxia in SIDS.Upsala journal of medical sciences · 2016Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
key pointsNeonatal sustained hypoxia exposure modifies brainstem microglia and serotonin expression. The altered brainstem neurochemistry is associated with impaired ventilatory responses to acute hypoxia and mortality. The deleterious effects of sustained hypoxia exposure can be prevented by an inhibitor of activated microglia. These observations demonstrate a potential cause of the brainstem serotonin abnormalities thought to be involved in sudden infant death syndrome. ABSTRACT: We showed previously that the end of the second postnatal week (days P11-15) represents a period of development during which the respiratory neural control system exhibits a heightened vulnerability to sustained hypoxia (SH, 11% O2 , 5 days) exposure. In the current study, we investigated whether the vulnerability to SH during the same developmental time period is associated with changes in brainstem serotonin (5-HT) expression and whether it can be prevented by the microglia inhibitor minocycline. Using whole-body plethysmography, SH attenuated the acute (5 min) hypoxic ventilatory response (HVR) and caused a high incidence of mortality compared to normoxia rats. SH also increased microglia cell numbers and decreased 5-HT immunoreactivity in the nucleus of the solitary tract (nTS) and dorsal motor nucleus of the vagus (DMNV). The attenuated HVR, mortality, and changes in nTS and DMNV immunoreactivity was prevented by minocycline (25 mg kg(-1) /2 days during SH). These data demonstrate that the 5-HT abnormalities in distinct respiratory neural control regions can be initiated by prolonged hypoxia exposure and may be modulated by microglia activity. These observations share several commonalities with the risk factors thought to underlie the aetiology of sudden infant death syndrome, including: (1) a vulnerable neonate; (2) a critical period of development; (3) evidence of hypoxia; (4) brainstem gliosis (particularly the nTS and DMNV); and (5) 5-HT abnormalities.
Indexed as
Identifiers
What OpenQuestion holds
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.