ReviewThe Journal of physiology2009
NADPH oxidase activity is necessary for acute intermittent hypoxia-induced phrenic long-term facilitation.
Review in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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The trial behind it
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Who cites it
54 citing papers in PubMed, 75 citations in OpenAlex.
- Progressive augmentation and ventilatory long-term facilitation are enhanced in sleep apnoea patients and are mitigated by antioxidant administration.The Journal of physiology · 2009Trial
- The development but not the maintenance of phrenic and sympathetic long-term facilitation after acute intermittent hypoxia requires nucleus tractus solitarii HExperimental neurology · 2025Article
- Daily acute intermittent hypoxia elicits age & sex-dependent changes in molecules regulating phrenic motor plasticity.Experimental neurology · 2025Article
- Microglia regulate motor neuron plasticity via reciprocal fractalkine and adenosine signaling.Nature communications · 2024Article
- Inactivity-induced phrenic motor facilitation requires PKCζ activity within phrenic motor neurons.Journal of neurophysiology · 2024Article
- Microglia regulate motor neuron plasticity via reciprocal fractalkine/adenosine signaling.bioRxiv : the preprint server for biology · 2024Article
- Therapeutic acute intermittent hypoxia: A translational roadmap for spinal cord injury and neuromuscular disease.Experimental neurology · 2022Review
- Divergent receptor utilization is necessary for phrenic long-term facilitation over the course of motor neuron loss following CTB-SAP intrapleural injections.Journal of neurophysiology · 2021Article
- Acute morphine blocks spinal respiratory motor plasticity via long-latency mechanisms that require toll-like receptor 4 signalling.The Journal of physiology · 2021Article
- Mechanisms of severe acute intermittent hypoxia-induced phrenic long-term facilitation.Journal of neurophysiology · 2021Article
- Systemic inflammation suppresses spinal respiratory motor plasticity via mechanisms that require serine/threonine protein phosphatase activity.Journal of neuroinflammation · 2021Article
- Impact of inflammation on developing respiratory control networks: rhythm generation, chemoreception and plasticity.Respiratory physiology & neurobiology · 2020Review
- Cervical spinal 5-HTJournal of applied physiology (Bethesda, Md. : 1985) · 2019Article
- Competing mechanisms of plasticity impair compensatory responses to repetitive apnoea.The Journal of physiology · 2019Article
- Circulatory control of phrenic motor plasticity.Respiratory physiology & neurobiology · 2019Review
- Protein kinase Cδ constrains the S-pathway to phrenic motor facilitation elicited by spinal 5-HTThe Journal of physiology · 2019Article
- The Plasma Membrane: A Platform for Intra- and Intercellular Redox Signaling.Antioxidants (Basel, Switzerland) · 2018Review
- Intermittent but not sustained moderate hypoxia elicits long-term facilitation of hypoglossal motor output.Respiratory physiology & neurobiology · 2018Article
- Pharmacological modulation of hypoxia-induced respiratory neuroplasticity.Respiratory physiology & neurobiology · 2018Review
- Cross-talk inhibition between 5-HTAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Phrenic long-term facilitation (pLTF) following acute intermittent hypoxia (AIH) is a form of spinal, serotonin-dependent synaptic plasticity that requires reactive oxygen species (ROS) formation. We tested the hypothesis that spinal NADPH oxidase activity is a necessary source of ROS for pLTF. Sixty minutes post-AIH (three 5-min episodes of 11% O(2), 5 min intervals), integrated phrenic and hypoglossal (XII) nerve burst amplitudes were increased from baseline, indicative of phrenic and XII LTF. Intrathecal injections (approximately C(4)) of apocynin or diphenyleneiodonium chloride (DPI), two structurally and functionally distinct inhibitors of the NADPH oxidase complex, attenuated phrenic, but not XII, LTF. Immunoblots from soluble (cytosolic) and particulate (membrane) fractions of ventral C(4) spinal segments revealed predominantly membrane localization of the NADPH oxidase catalytic subunit, gp91(phox), whereas membrane and cytosolic expression were both observed for the regulatory subunits, p47(phox) and RAC1. Immunohistochemical analysis of fixed tissues revealed these same subunits in presumptive phrenic motoneurons of the C(4) ventral horn, but not in neighbouring astrocytes or microglia. Collectively, these data demonstrate that NADPH oxidase subunits localized within presumptive phrenic motoneurons are a major source of ROS necessary for AIH-induced pLTF. Thus, NADPH oxidase activity is a key regulator of spinal synaptic plasticity, and may be a useful pharmaceutical target in developing therapeutic strategies for respiratory insufficiency in patients with, for example, cervical spinal injury.
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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.