ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Intermittent Hypoxia-Induced Spinal Inflammation Impairs Respiratory Motor Plasticity by a Spinal p38 MAP Kinase-Dependent Mechanism.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 75 citations in OpenAlex.
- Vagal suppression of diurnal variations in acute intermittent hypoxia-induced phrenic long-term facilitation.Journal of neurophysiology · 2026Article
- Persistent suppression of phrenic motor plasticity after mild acute systemic inflammation in adult rats.Function (Oxford, England) · 2026Article
- Neonatal inflammation induces lasting sex- and region-dependent microglia activation and sex-dependent impairments in chemoreflexes.Journal of applied physiology (Bethesda, Md. : 1985) · 2026Article
- Plasticity induced loss of apnea alarm through repeated apneas: A proposed mechanism for respiratory sudden death.Epilepsy & behavior : E&B · 2025Review
- Daily acute intermittent hypoxia elicits age & sex-dependent changes in molecules regulating phrenic motor plasticity.Experimental neurology · 2025Article
- Sex andJournal of neurophysiology · 2024Article
- Microglia and Sleep Disorders.Advances in neurobiology · 2024Review
- Mild inflammation impairs acute intermittent hypoxia-induced phrenic long-term facilitation by a spinal adenosine-dependent mechanism.Journal of neurophysiology · 2023Article
- APOE4, Age & Sex Regulate Respiratory Plasticity Elicited By Acute Intermittent Hypercapnic-Hypoxia.bioRxiv : the preprint server for biology · 2023Article
- APOE4, Age, and Sex Regulate Respiratory Plasticity Elicited by Acute Intermittent Hypercapnic-Hypoxia.Function (Oxford, England) · 2023Article
- Fractalkine/CX3CR1-Dependent Modulation of Synaptic and Network Plasticity in Health and Disease.Neural plasticity · 2023Review
- Role of microglia in blood pressure and respiratory responses to acute hypoxic exposure in rats.The journal of physiological sciences : JPS · 2022Article
- Dose-dependent phosphorylation of endogenous Tau by intermittent hypoxia in rat brain.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- Therapeutic acute intermittent hypoxia: A translational roadmap for spinal cord injury and neuromuscular disease.Experimental neurology · 2022Review
- Daily acute intermittent hypoxia enhances serotonergic innervation of hypoglossal motor nuclei in rats with and without cervical spinal injury.Experimental neurology · 2022Article
- Nonsteroidal anti-inflammatory drug (ketoprofen) delivery differentially impacts phrenic long-term facilitation in rats with motor neuron death induced by intrapleural CTB-SAP injections.Experimental neurology · 2022Article
- Acute morphine blocks spinal respiratory motor plasticity via long-latency mechanisms that require toll-like receptor 4 signalling.The Journal of physiology · 2021Article
- Protocol-Specific Effects of Intermittent Hypoxia Pre-Conditioning on Phrenic Motor Plasticity in Rats with Chronic Cervical Spinal Cord Injury.Journal of neurotrauma · 2021Article
- Serotonergic innervation of respiratory motor nuclei after cervical spinal injury: Impact of intermittent hypoxia.Experimental neurology · 2021Review
- Research Priorities for Patients with Heart Failure and Central Sleep Apnea. An Official American Thoracic Society Research Statement.American journal of respiratory and critical care medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation is characteristic of most clinical disorders that challenge the neural control of breathing. Since inflammation modulates neuroplasticity, we studied the impact of inflammation caused by prolonged intermittent hypoxia on an important form of respiratory plasticity, acute intermittent hypoxia (three, 5 min hypoxic episodes, 5 min normoxic intervals) induced phrenic long-term facilitation (pLTF). Because chronic intermittent hypoxia elicits neuroinflammation and pLTF is undermined by lipopolysaccharide-induced systemic inflammation, we hypothesized that one night of intermittent hypoxia (IH-1) elicits spinal inflammation, thereby impairing pLTF by a p38 MAP kinase-dependent mechanism. pLTF and spinal inflammation were assessed in anesthetized rats pretreated with IH-1 (2 min hypoxia, 2 min normoxia; 8 h) or sham normoxia and allowed 16 h for recovery. IH-1 (1) transiently increased IL-6 (1.5 ± 0.2-fold; p = 0.02) and inducible nitric oxide synthase (iNOS) (2.4 ± 0.4-fold; p = 0.01) mRNA in cervical spinal homogenates, (2) elicited a sustained increase in IL-1β mRNA (2.4 ± 0.2-fold; p < 0.001) in isolated cervical spinal microglia, and (3) abolished pLTF (-1 ± 5% vs 56 ± 10% in controls; p < 0.001). pLTF was restored after IH-1 by systemic NSAID administration (ketoprofen; 55 ± 9%; p < 0.001) or spinal p38 MAP kinase inhibition (58 ± 2%; p < 0.001). IH-1 increased phosphorylated (activated) p38 MAP kinase immunofluorescence in identified phrenic motoneurons and adjacent microglia. In conclusion, IH-1 elicits spinal inflammation and impairs pLTF by a spinal p38 MAP kinase-dependent mechanism. By targeting inflammation, we may develop strategies to manipulate respiratory motor plasticity for therapeutic advantage when the respiratory control system is compromised (e.g., sleep apnea, apnea of prematurity, spinal injury, or motor neuron disease).
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.