ArticleJournal of applied physiology (Bethesda, Md. : 1985)2014
Adrenergic α₁ receptor activation is sufficient, but not necessary for phrenic long-term facilitation.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- The hypoxic ventilatory response and arousal burden predict the magnitude of ventilatory long-term facilitation in humans with obstructive sleep apnoea.Experimental physiology · 2026Pooled it
- Acute intermittent hypoxia enhances nucleus of the solitary tract neuronal activity and requires NMDARs and CaMKII for phrenic long-term facilitation.Journal of neurophysiology · 2025Article
- Identification of multiple hypoxia-independent triggers of upper airway long-term facilitation in a rat model of upper airway motor plasticity.Physiological reports · 2025Article
- Daily acute intermittent hypoxia enhances serotonergic innervation of hypoglossal motor nuclei in rats with and without cervical spinal injury.Experimental neurology · 2022Article
- Mechanisms of severe acute intermittent hypoxia-induced phrenic long-term facilitation.Journal of neurophysiology · 2021Article
- Differential mechanisms are required for phrenic long-term facilitation over the course of motor neuron loss following CTB-SAP intrapleural injections.Experimental neurology · 2020Article
- Hypoxia-induced hypotension elicits adenosine-dependent phrenic long-term facilitation after carotid denervation.Experimental neurology · 2020Article
- Respiratory pattern and phrenic and hypoglossal nerve activity during normoxia and hypoxia in 6-OHDA-induced bilateral model of Parkinson's disease.The journal of physiological sciences : JPS · 2020Article
- Cervical spinal 5-HTJournal of applied physiology (Bethesda, Md. : 1985) · 2019Article
- Mechanisms of compensatory plasticity for respiratory motor neuron death.Respiratory physiology & neurobiology · 2019Review
- 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
- Brainstem Nuclei Associated with Mediating Apnea-Induced Respiratory Motor Plasticity.Scientific reports · 2018Article
- Noradrenergic Activation of Hypoglossal Nucleus Modulates the Central Regulation of Genioglossus in Chronic Intermittent Hypoxic Rats.Frontiers in neurology · 2017Article
- Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis.Comprehensive Physiology · 2016Review
- Repetitive acute intermittent hypoxia increases growth/neurotrophic factor expression in non-respiratory motor neurons.Neuroscience · 2016Article
- Spinal metaplasticity in respiratory motor control.Frontiers in neural circuits · 2015Review
- Therapeutic acute intermittent hypoxia modestly improves breathing in Pompe disease.Respiratory physiology & neurobiologyArticle
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Acute intermittent hypoxia (AIH; three 5-min hypoxic episodes) causes a form of phrenic motor facilitation (pMF) known as phrenic long-term facilitation (pLTF); pLTF is initiated by spinal activation of Gq protein-coupled 5-HT2 receptors. Because α1 adrenergic receptors are expressed in the phrenic motor nucleus and are also Gq protein-coupled, we hypothesized that α1 receptors are sufficient, but not necessary for AIH-induced pLTF. In anesthetized, paralyzed, and ventilated rats, episodic spinal application of the α1 receptor agonist phenylephrine (PE) elicited dose-dependent pMF (10 and 100 μM, P < 0.05; but not 1 μM). PE-induced pMF was blocked by the α1 receptor antagonist prazosin (1 mM; -20 ± 20% at 60 min, -5 ± 21% at 90 min; n = 6). Although α1 receptor activation is sufficient to induce pMF, it was not necessary for AIH-induced pLTF because intrathecal prazosin (1 mM) did not alter AIH-induced pLTF (56 ± 9% at 60 min, 78 ± 12% at 90 min; n = 9). Intravenous (iv) prazosin (150 μg/kg) appeared to reduce pLTF (21 ± 9% at 60 min, 26 ± 8% at 90 min), but this effect was not significant. Hypoglossal long-term facilitation was unaffected by intrathecal prazosin, but was blocked by iv prazosin (-4 ± 14% at 60 min, -13 ± 18% at 90 min), suggesting different LTF mechanisms in different motor neuron pools. In conclusion, Gq protein-coupled α1 adrenergic receptors evoke pMF, but they are not necessary for AIH-induced pLTF.
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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.