ArticleJournal of neurophysiology2015
Mammalian target of rapamycin is required for phrenic long-term facilitation following severe but not moderate acute intermittent hypoxia.
Article in Journal of neurophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Sexual dimorphisms in phrenic long-term facilitation following severe acute intermittent hypoxia.Journal of neurophysiology · 2026Article
- Phrenic long-term facilitation following severe acute intermittent hypoxia is preserved in geriatric male rats.Journal of neurophysiology · 2025Article
- Plasticity induced loss of apnea alarm through repeated apneas: A proposed mechanism for respiratory sudden death.Epilepsy & behavior : E&B · 2025Review
- Low level CORespiratory physiology & neurobiology · 2024Article
- High frequency repetitive Transcranial Magnetic Stimulation promotes long lasting phrenic motoneuron excitability via GABAergic networks.Respiratory physiology & neurobiology · 2021Article
- The long-term impact of ovariectomy on ventilation and expression of phrenic long-term facilitation in female rats.Experimental physiology · 2021Article
- Cervical spinal injury compromises caudal spinal tissue oxygenation and undermines acute intermittent hypoxia-induced phrenic long-term facilitation.Experimental neurology · 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
- Mechanisms of severe acute intermittent hypoxia-induced phrenic long-term facilitation.Journal of neurophysiology · 2021Article
- Impact of inflammation on developing respiratory control networks: rhythm generation, chemoreception and plasticity.Respiratory physiology & neurobiology · 2020Review
- Spinal AMP kinase activity differentially regulates phrenic motor plasticity.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Cervical spinal 5-HTJournal of applied physiology (Bethesda, Md. : 1985) · 2019Article
- Pharmacological modulation of hypoxia-induced respiratory neuroplasticity.Respiratory physiology & neurobiology · 2018Review
- Daily acute intermittent hypoxia improves breathing function with acute and chronic spinal injury via distinct mechanisms.Respiratory physiology & neurobiology · 2018Article
- Article
- Nongenomic Actions of 17-β Estradiol Restore Respiratory Neuroplasticity in Young Ovariectomized Female Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Adenosine-dependent phrenic motor facilitation is inflammation resistant.Journal of neurophysiology · 2017Article
- Sustained Hypoxia Elicits Competing Spinal Mechanisms of Phrenic Motor Facilitation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
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3 authors.
Funding
Abstract
Phrenic long-term facilitation (pLTF) is a persistent increase in phrenic nerve activity after acute intermittent hypoxia (AIH). Distinct cell-signaling cascades give rise to pLTF depending on the severity of hypoxemia within hypoxic episodes. Moderate AIH (mAIH; three 5-min episodes, PaO2 ∼35-55 mmHG) elicits pLTF by a serotonin (5-HT)-dependent mechanism that requires new synthesis of brain-derived neurotrophic factor (BDNF), activation of its high-affinity receptor (TrkB), and ERK MAPK signaling. In contrast, severe AIH (sAIH; three 5-min episodes, PaO2 ∼25-30 mmHG) elicits pLTF by an adenosine-dependent mechanism that requires new TrkB synthesis and Akt signaling. Although both mechanisms require spinal protein synthesis, the newly synthesized proteins are distinct, as are the neurochemicals inducing plasticity (serotonin vs. adenosine). In many forms of neuroplasticity, new protein synthesis requires translational regulation via mammalian target of rapamycin (mTOR) signaling. Since Akt regulates mTOR activity, we hypothesized that mTOR activity is necessary for sAIH- but not mAIH-induced pLTF. Phrenic nerve activity in anesthetized, paralyzed, and ventilated rats was recorded before, during, and 60 min after mAIH or sAIH. Rats were pretreated with intrathecal injections of 20% DMSO (vehicle controls) or rapamycin (0.1 mM, 12 μl), a selective mTOR complex 1 inhibitor. Consistent with our hypothesis, rapamycin blocked sAIH- but not mAIH-induced pLTF. Thus spinal mTOR activity is required for adenosine-dependent (sAIH) but not serotonin-dependent (mAIH) pLTF, suggesting that distinct mechanisms regulate new protein synthesis in these forms of spinal neuroplasticity.
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