ArticleNeuroscience2013
Spinal 5-HT7 receptors and protein kinase A constrain intermittent hypoxia-induced phrenic long-term facilitation.
Article in Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- Amino acid modulation of the carotid body selectively modulates peripheral chemoreceptor respiratory reflex.The Journal of physiology · 2026Article
- Phrenic long-term facilitation following acute intermittent hypercapnic-hypoxia in rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Plasticity induced loss of apnea alarm through repeated apneas: A proposed mechanism for respiratory sudden death.Epilepsy & behavior : E&B · 2025Review
- Phrenic long-term facilitation following severe acute intermittent hypoxia is preserved in geriatric male rats.Journal of neurophysiology · 2025Article
- Targeting the serotonergic system in the treatment of neurodegenerative diseases-emerging therapies and unmet challenges.Pharmacological reviews · 2025Review
- Daily acute intermittent hypoxia elicits age & sex-dependent changes in molecules regulating phrenic motor plasticity.Experimental neurology · 2025Article
- Can Serotonin 7 Receptors Be a Treatment Target for Noncentral Diseases?The Eurasian journal of medicine · 2023Article
- Therapeutic acute intermittent hypoxia: A translational roadmap for spinal cord injury and neuromuscular disease.Experimental neurology · 2022Review
- Adenosine A2a receptors modulate TrkB receptor-dependent respiratory plasticity in neonatal rats.Respiratory physiology & neurobiology · 2021Article
- 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
- 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
- Spinal AMP kinase activity differentially regulates phrenic motor plasticity.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Circulatory control of phrenic motor plasticity.Respiratory physiology & neurobiology · 2019Review
- Increased tongue use enhances 5-HTRespiratory physiology & neurobiology · 2019Article
- Protein kinase Cδ constrains the S-pathway to phrenic motor facilitation elicited by spinal 5-HTThe Journal of physiology · 2019Article
- Daily acute intermittent hypoxia improves breathing function with acute and chronic spinal injury via distinct mechanisms.Respiratory physiology & neurobiology · 2018Article
- Phrenic long-term facilitation following intrapleural CTB-SAP-induced respiratory motor neuron death.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
2 authors at 1 institution in 1 country.
Funding
Abstract
Phrenic long-term facilitation (pLTF) is a form of serotonin-dependent respiratory plasticity induced by acute intermittent hypoxia (AIH). pLTF requires spinal Gq protein-coupled serotonin-2 receptor (5-HT2) activation, new synthesis of brain-derived neurotrophic factor (BDNF) and activation of its high-affinity receptor, TrkB. Intrathecal injections of selective agonists for Gs protein-coupled receptors (adenosine 2A and serotonin-7; 5-HT7) also induce long-lasting phrenic motor facilitation via TrkB "trans-activation." Since serotonin released near phrenic motor neurons may activate multiple serotonin receptor subtypes, we tested the hypothesis that 5-HT7 receptor activation contributes to AIH-induced pLTF. A selective 5-HT7 receptor antagonist (SB-269970, 5mM, 12 μl) was administered intrathecally at C4 to anesthetized, vagotomized and ventilated rats prior to AIH (3, 5-min episodes, 11% O2). Contrary to predictions, pLTF was greater in SB-269970 treated versus control rats (80 ± 11% versus 45 ± 6% 60 min post-AIH; p<0.05). Hypoglossal LTF was unaffected by spinal 5-HT7 receptor inhibition, suggesting that drug effects were localized to the spinal cord. Since 5-HT7 receptors are coupled to protein kinase A (PKA), we tested the hypothesis that PKA inhibits AIH-induced pLTF. Similar to 5-HT7 receptor inhibition, spinal PKA inhibition (KT-5720, 100 μM, 15 μl) enhanced pLTF (99 ± 15% 60 min post-AIH; p<0.05). Conversely, PKA activation (8-br-cAMP, 100 μM, 15 μl) blunted pLTF versus control rats (16 ± 5% versus 45 ± 6% 60 min post-AIH; p<0.05). These findings suggest a novel mechanism whereby spinal Gs protein-coupled 5-HT7 receptors constrain AIH-induced pLTF via PKA activity.
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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.