ArticleeLife2023
Opioid suppression of an excitatory pontomedullary respiratory circuit by convergent mechanisms.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Partially countering the physiological effects of fentanyl with naloxone or d-cysteine ethyl ester in adult goats.Journal of applied physiology (Bethesda, Md. : 1985) · 2026Article
- A projection atlas of excitatory and inhibitory inputs to the preBötzinger complex: substrates for multimodal breathing control.Journal of neurophysiology · 2026Article
- Melanocortin receptor 4 agonist setmelanotide treats opioid-induced respiratory depression.bioRxiv : the preprint server for biology · 2026Article
- Acute fentanyl and xylazine co-exposure uniquely increase the excitability of dopamine type 2 receptor-expressing striatal medium spiny neurons.Journal of neurophysiology · 2026Article
- Brain-wide mapping of acute hypoxia-induced neuronal activation in mice: A c-Fos immunofluorescence study.IBRO neuroscience reports · 2025Article
- Multimodal Breathing Control: Pontomedullary Mechanisms and Current Perspectives.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Functional modulation of retrotrapezoid neurons drives fentanyl-induced respiratory depression.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Xylazine exacerbates fentanyl-induced respiratory depression and bradycardia.The Journal of pharmacology and experimental therapeutics · 2025Article
- Reversal of morphine-induced respiratory depression with the µAmerican journal of physiology. Lung cellular and molecular physiology · 2025Article
- Different effects of epidural versus paravertebral analgesia on respiratory rate variability after oesophagectomy: A single-centre observational subanalysis from the PEPMEN trial.European journal of anaesthesiology and intensive care · 2025Article
- Article
- Sustained fentanyl exposure inhibits neuronal activity in dissociated striatal neuronal-glial cocultures through actions independent of opioid receptors.Journal of neurophysiology · 2024Article
- Opioid-induced respiratory depression.BJA education · 2024Review
- Editorial: Opioid-induced respiratory depression: neural circuits and cellular pathways.Frontiers in physiology · 2023Article
- Fentanyl effects on respiratory neuron activity in the dorsolateral pons.Journal of neurophysiology · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Opioids depress breathing by inhibition of interconnected respiratory nuclei in the pons and medulla. Mu opioid receptor (MOR) agonists directly hyperpolarize a population of neurons in the dorsolateral pons, particularly the Kölliker-Fuse (KF) nucleus, that are key mediators of opioid-induced respiratory depression. However, the projection target and synaptic connections of MOR-expressing KF neurons are unknown. Here, we used retrograde labeling and brain slice electrophysiology to determine that MOR-expressing KF neurons project to respiratory nuclei in the ventrolateral medulla, including the preBötzinger complex (preBötC) and rostral ventral respiratory group (rVRG). These medullary-projecting, MOR-expressing dorsolateral pontine neurons express FoxP2 and are distinct from calcitonin gene-related peptide-expressing lateral parabrachial neurons. Furthermore, dorsolateral pontine neurons release glutamate onto excitatory preBötC and rVRG neurons via monosynaptic projections, which is inhibited by presynaptic opioid receptors. Surprisingly, the majority of excitatory preBötC and rVRG neurons receiving MOR-sensitive glutamatergic synaptic input from the dorsolateral pons are themselves hyperpolarized by opioids, suggesting a selective opioid-sensitive circuit from the KF to the ventrolateral medulla. Opioids inhibit this excitatory pontomedullary respiratory circuit by three distinct mechanisms-somatodendritic MORs on dorsolateral pontine and ventrolateral medullary neurons and presynaptic MORs on dorsolateral pontine neuron terminals in the ventrolateral medulla-all of which could contribute to opioid-induced respiratory depression.
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What Socratic holds
Registered trials
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 Socratic graph.