ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Spinal atypical protein kinase C activity is necessary to stabilize inactivity-induced phrenic motor facilitation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Quantitative assessment of integrated phrenic nerve activity.Respiratory physiology & neurobiology · 2016Pooled it
- Intermittent phrenic afferent activation induces phrenic motor plasticity.Journal of neurophysiology · 2026Article
- Inactivity-induced phrenic motor facilitation requires PKCζ activity within phrenic motor neurons.Journal of neurophysiology · 2024Article
- Retinoic acid receptor alpha activation is necessary and sufficient for plasticity induced by recurrent central apnea.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Baseline Arterial COFrontiers in physiology · 2021Article
- Competing mechanisms of plasticity impair compensatory responses to repetitive apnoea.The Journal of physiology · 2019Article
- Spinal activation of protein kinase C elicits phrenic motor facilitation.Respiratory physiology & neurobiology · 2018Article
- Intermittent apnea elicits inactivity-induced phrenic motor facilitation via a retinoic acid- and protein synthesis-dependent pathway.Journal of neurophysiology · 2017Article
- Coupling multielectrode array recordings with silver labeling of recording sites to study cervical spinal network connectivity.Journal of neurophysiology · 2017Article
- Plasticity in respiratory motor neurons in response to reduced synaptic inputs: A form of homeostatic plasticity in respiratory control?Experimental neurology · 2017Review
- Reduced respiratory neural activity elicits a long-lasting decrease in the COExperimental neurology · 2017Article
- Phrenic long-term facilitation requires PKCθ activity within phrenic motor neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Intermittent reductions in respiratory neural activity elicit spinal TNF-α-independent, atypical PKC-dependent inactivity-induced phrenic motor facilitation.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Spinal NMDA receptor activation constrains inactivity-induced phrenic motor facilitation in Charles River Sprague-Dawley rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- Neither serotonin nor adenosine-dependent mechanisms preserve ventilatory capacity in ALS rats.Respiratory physiology & neurobiology · 2014Article
- Decreased spinal synaptic inputs to phrenic motor neurons elicit localized inactivity-induced phrenic motor facilitation.Experimental neurology · 2014Article
- Spinal TNF is necessary for inactivity-induced phrenic motor facilitation.The Journal of physiology · 2013Article
- Inactivity-induced respiratory plasticity: protecting the drive to breathe in disorders that reduce respiratory neural activity.Respiratory physiology & neurobiology · 2013Review
- Inactivity-induced phrenic and hypoglossal motor facilitation are differentially expressed following intermittent vs. sustained neural apnea.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
- Hypoxia-induced phrenic long-term facilitation: emergent properties.Annals of the New York Academy of Sciences · 2013Review
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Authors and funding
5 authors.
Funding
Abstract
The neural network controlling breathing must establish rhythmic motor output at a level adequate to sustain life. Reduced respiratory neural activity elicits a novel form of plasticity in circuits driving the diaphragm known as inactivity-induced phrenic motor facilitation (iPMF), a rebound increase in phrenic inspiratory output observed once respiratory neural drive is restored. The mechanisms underlying iPMF are unknown. Here, we demonstrate in anesthetized rats that spinal mechanisms give rise to iPMF and that iPMF consists of at least two mechanistically distinct phases: (1) an early, labile phase that requires atypical PKC (PKCζ and/or PKCι/λ) activity to transition to a (2) late, stable phase. Early (but not late) iPMF is associated with increased interactions between PKCζ/ι and the scaffolding protein ZIP (PKCζ-interacting protein)/p62 in spinal regions associated with the phrenic motor pool. Although PKCζ/ι activity is necessary for iPMF, spinal atypical PKC activity is not necessary for phrenic long-term facilitation (pLTF) following acute intermittent hypoxia, an activity-independent form of spinal respiratory plasticity. Thus, while iPMF and pLTF both manifest as prolonged increases in phrenic burst amplitude, they arise from distinct spinal cellular pathways. Our data are consistent with the hypotheses that (1) local mechanisms sense and respond to reduced respiratory-related activity in the phrenic motor pool and (2) inactivity-induced increases in phrenic inspiratory output require local PKCζ/ι activity to stabilize into a long-lasting iPMF. Although the physiological role of iPMF is unknown, we suspect that iPMF represents a compensatory mechanism, assuring adequate motor output in a physiological system in which prolonged inactivity ends life.
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