ArticleFrontiers in molecular neuroscience2022
Nucleus Tractus Solitarius Neurons Activated by Hypercapnia and Hypoxia Lack Mu Opioid Receptor Expression.
Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Hypothalamic Glutamatergic/Orexinergic Neurons Attenuate Fentanyl-Induced Respiratory Depression via Medullary Pre-BöTzinger Complex Pathways.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Functional modulation of retrotrapezoid neurons drives fentanyl-induced respiratory depression.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Article
- Respiratory Depression Associated with Opioids: A Narrative Review.Current treatment options in oncology · 2024Review
- Article
- Prospective case-control study on pain intensity after the use of promethazine in patients undergoing videothoracoscopy.Frontiers in medicine · 2024Article
- Human OPRM1 and murine Oprm1 promoter driven viral constructs for genetic access to μ-opioidergic cell types.Nature communications · 2023Article
- Opioid suppression of an excitatory pontomedullary respiratory circuit by convergent mechanisms.eLife · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Impaired chemoreflex responses are a central feature of opioid-induced respiratory depression, however, the mechanism through which mu opioid receptor agonists lead to diminished chemoreflexes is not fully understood. One brainstem structure involved in opioid-induced impairment of chemoreflexes is the nucleus of the solitary tract (NTS), which contains a population of neurons that express mu opioid receptors. Here, we tested whether caudal NTS neurons activated during the chemoreflex challenge express mu opioid receptors and overlap with neurons activated by opioids. Using genetic labeling of mu opioid receptor-expressing neurons and cFos immunohistochemistry as a proxy for neuronal activation, we examined the distribution of activated NTS neurons following hypercapnia, hypoxia, and morphine administration. The main finding was that hypoxia and hypercapnia primarily activated NTS neurons that did not express mu opioid receptors. Furthermore, concurrent administration of morphine with hypercapnia induced cFos expression in non-overlapping populations of neurons. Together these results suggest an indirect effect of opioids within the NTS, which could be mediated through mu opioid receptors on afferents and/or inhibitory interneurons.
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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 OpenQuestion graph.