ArticleScientific reports2016
Contribution of the respiratory network to rhythm and motor output revealed by modulation of GIRK channels, somatostatin and neurokinin-1 receptors.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Comparative Ion Channel Transcriptomes of NK1R and Somatostatin Neurons in the PreBötzinger Complex of the Ventrolateral Medulla.Molecular neurobiology · 2026Article
- Comparative Ion Channel Transcriptomes of NK1R and Somatostatin Neurons in the preBötzinger Complex of the Ventrolateral Medulla.Research square · 2026Article
- Modeling insights into potential mechanisms of opioid-induced respiratory depression within medullary and pontine networks.Journal of neurophysiology · 2026Article
- Characterisation of sleep apneas and respiratory circuitry in mice lacking CDKL5.Journal of sleep research · 2025Article
- Cholinergic modulation of upper airway control: maturational changes and mechanisms at cellular and synaptic levels.Journal of neurophysiology · 2025Review
- Endomorphin-2 (Endo2) and substance P (SubP) co-application attenuates SubP-induced excitation and alters frequency plasticity in neonatal rat in vitro preparations.Respiratory physiology & neurobiology · 2025Article
- Human IPSC-Derived PreBötC-Like Neurons and Development of an Opiate Overdose and Recovery Model.Advanced biology · 2024Article
- Chronic intermittent hypoxia elicits distinct transcriptomic responses among neurons and oligodendrocytes within the brainstem of mice.American journal of physiology. Lung cellular and molecular physiology · 2024Article
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- βγ G-proteins, but not regulators of G-protein signaling 4, modulate opioid-induced respiratory rate depression.Frontiers in physiology · 2023Article
- Mechanisms of opioid-induced respiratory depression.Archives of toxicology · 2022Review
- Current research in pathophysiology of opioid-induced respiratory depression, neonatal opioid withdrawal syndrome, and neonatal antidepressant exposure syndrome.Current research in toxicology · 2022Article
- Toxicities of opioid analgesics: respiratory depression, histamine release, hemodynamic changes, hypersensitivity, serotonin toxicity.Archives of toxicology · 2021Review
- Neuronal mechanisms underlying opioid-induced respiratory depression: our current understanding.Journal of neurophysiology · 2021Review
- Measurement and State-Dependent Modulation of Hypoglossal Motor Excitability and Responsivity In-Vivo.Scientific reports · 2020Article
- Differential impact of two critical respiratory centres in opioid-induced respiratory depression in awake mice.The Journal of physiology · 2020Article
- Presynaptic Mechanisms and KCNQ Potassium Channels Modulate Opioid Depression of Respiratory Drive.Frontiers in physiology · 2019Article
- δ-Subunit Containing GABAScientific reports · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breathing is generated by a respiratory network in the brainstem. At its core, a population of neurons expressing neurokinin-1 receptors (NK1R) and the peptide somatostatin (SST) form the preBötzinger Complex (preBötC), a site essential for the generation of breathing. PreBötC interneurons generate rhythm and follower neurons shape motor outputs by activating upper airway respiratory muscles. Since NK1R-expressing preBötC neurons are preferentially inhibited by μ-opioid receptors via activation of GIRK channels, NK1R stimulation may also involve GIRK channels. Hence, we identify the contribution of GIRK channels to rhythm, motor output and respiratory modulation by NK1Rs and SST. In adult rats, GIRK channels were identified in NK1R-expressing preBötC cells. Their activation decreased breathing rate and genioglossus muscle activity, an important upper airway muscle. NK1R activation increased rhythmic breathing and genioglossus muscle activity in wild-type mice, but not in mice lacking GIRK2 subunits (GIRK2(-/-)). Conversely, SST decreased rhythmic breathing via SST2 receptors, reduced genioglossus muscle activity likely through SST4 receptors, but did not involve GIRK channels. In summary, NK1R stimulation of rhythm and motor output involved GIRK channels, whereas SST inhibited rhythm and motor output via two SST receptor subtypes, therefore revealing separate circuits mediating rhythm and motor output.
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