ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Phrenic long-term facilitation requires PKCθ activity within phrenic motor neurons.
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 57 papers.
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Who cites it
57 citing papers in PubMed, 67 citations in OpenAlex.
- Circadian clock protein Bmal1 regulates respiratory motor plasticity in male rats.Function (Oxford, England) · 2026Article
- Vagal suppression of diurnal variations in acute intermittent hypoxia-induced phrenic long-term facilitation.Journal of neurophysiology · 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
- Diurnal cycle and acute intermittent hypoxia protocol interact to regulate ventilatory long-term facilitation in unanesthetized rats.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
- Identification of multiple hypoxia-independent triggers of upper airway long-term facilitation in a rat model of upper airway motor plasticity.Physiological reports · 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
- Spinal TNF-α receptor 1 is differentially required for phrenic long-term facilitation (pLTF) over the course of motor neuron death in adult rats.Frontiers in physiology · 2024Article
- Increased spinal adenosine impairs phrenic long-term facilitation in aging rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- BDNF-induced phrenic motor facilitation shifts from PKCθ to ERK dependence with mild systemic inflammation.Journal of neurophysiology · 2023Article
- Targeting drug or gene delivery to the phrenic motoneuron pool.Journal of neurophysiology · 2023Review
- Nucleus tractus solitarii is required for the development and maintenance of phrenic and sympathetic long-term facilitation after acute intermittent hypoxia.Frontiers in physiology · 2023Article
- Acute intermittent hypercapnic-hypoxia elicits central neural respiratory motor plasticity in humans.The Journal of physiology · 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
- 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
- Daily acute intermittent hypoxia enhances phrenic motor output and stimulus-evoked phrenic responses in rats.Journal of neurophysiology · 2021Article
- How Are Adenosine and Adenosine ABiomedicines · 2021Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Acute intermittent hypoxia (AIH) induces a form of spinal motor plasticity known as phrenic long-term facilitation (pLTF); pLTF is a prolonged increase in phrenic motor output after AIH has ended. In anesthetized rats, we demonstrate that pLTF requires activity of the novel PKC isoform, PKCθ, and that the relevant PKCθ is within phrenic motor neurons. Whereas spinal PKCθ inhibitors block pLTF, inhibitors targeting other PKC isoforms do not. PKCθ is highly expressed in phrenic motor neurons, and PKCθ knockdown with intrapleural siRNAs abolishes pLTF. Intrapleural siRNAs targeting PKCζ, an atypical PKC isoform expressed in phrenic motor neurons that underlies a distinct form of phrenic motor plasticity, does not affect pLTF. Thus, PKCθ plays a critical role in spinal AIH-induced respiratory motor plasticity, and the relevant PKCθ is localized within phrenic motor neurons. Intrapleural siRNA delivery has considerable potential as a therapeutic tool to selectively manipulate plasticity in vital respiratory motor neurons.
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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.