ArticleJournal of neurophysiology2010
Clinically relevant infusion rates of mu-opioid agonist remifentanil cause bradypnea in decerebrate dogs but not via direct effects in the pre-Bötzinger complex region.
Article in Journal of neurophysiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- Asymmetric neuromodulation in the respiratory network contributes to rhythm and pattern generation.Frontiers in neural circuits · 2025Article
- Human IPSC-Derived PreBötC-Like Neurons and Development of an Opiate Overdose and Recovery Model.Advanced biology · 2024Article
- Changes in pontine and preBötzinger/Bötzinger complex neuronal activity during remifentanil-induced respiratory depression in decerebrate dogs.Frontiers in physiology · 2023Article
- Opioids, sleep, analgesia and respiratory depression: Their convergence on Mu (μ)-opioid receptors in the parabrachial area.Frontiers in neuroscience · 2023Review
- Mechanisms of opioid-induced respiratory depression.Archives of toxicology · 2022Review
- Contribution of the caudal medullary raphe to opioid induced respiratory depression.Respiratory physiology & neurobiology · 2022Article
- Current research in pathophysiology of opioid-induced respiratory depression, neonatal opioid withdrawal syndrome, and neonatal antidepressant exposure syndrome.Current research in toxicology · 2022Article
- Mu-opioid receptor-dependent transformation of respiratory motor pattern in neonatesFrontiers in physiology · 2022Article
- Dose-dependent Respiratory Depression by Remifentanil in the Rabbit Parabrachial Nucleus/Kölliker-Fuse Complex and Pre-Bötzinger Complex.Anesthesiology · 2021Article
- Dual mechanisms of opioid-induced respiratory depression in the inspiratory rhythm-generating network.eLife · 2021Article
- Toxicities of opioid analgesics: respiratory depression, histamine release, hemodynamic changes, hypersensitivity, serotonin toxicity.Archives of toxicology · 2021Review
- Neural basis of opioid-induced respiratory depression and its rescue.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Neuronal mechanisms underlying opioid-induced respiratory depression: our current understanding.Journal of neurophysiology · 2021Review
- Multi-Level Regulation of Opioid-Induced Respiratory Depression.Physiology (Bethesda, Md.) · 2020Review
- Kölliker-Fuse/Parabrachial complex mu opioid receptors contribute to fentanyl-induced apnea and respiratory rate depression.Respiratory physiology & neurobiology · 2020Article
- Article
- 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
- Julius H. Comroe Distinguished Lecture: Interdependence of neuromodulators in the control of breathing.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Review
- Ventilation and neurochemical changes during µ-opioid receptor activation or blockade of excitatory receptors in the hypoglossal motor nucleus of goats.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Systemic administration of mu-opioids at clinical doses for analgesia typically slows respiratory rate. Mu-opioid receptors (MORs) on pre-Bötzinger Complex (pre-BötC) respiratory neurons, the putative kernel of respiratory rhythmogenesis, are potential targets. The purpose of this study was to determine the contribution of pre-BötC MORs to the bradypnea produced in vivo by intravenous administration of clinically relevant infusion rates of remifentanil (remi), a short-acting, potent mu-opioid analgesic. In decerebrate dogs, multibarrel micropipettes were used to record pre-BötC neuronal activity and to eject the opioid antagonist naloxone (NAL, 0.5 mM), the glutamate agonist D-homocysteic acid (DLH, 20 mM), or the MOR agonist [D-Ala(2), N-Me-Phe(4), gly-ol(5)]-enkephalin (DAMGO, 100 microM). Inspiratory and expiratory durations (T(I) and T(E)) and peak phrenic nerve activity (PPA) were measured from the phrenic neurogram. The pre-BötC was functionally identified by its rate altering response (typically tachypnea) to DLH microinjection. During intravenous remi-induced bradypnea (approximately 60% decrease in central breathing frequency, f(B)), bilateral injections of NAL in the pre-BötC did not change T(I), T(E), f(B), and PPA. Also, NAL picoejected onto single pre-BötC neurons depressed by intravenous remi had no effect on their discharge. In contrast, approximately 60 microg/kg of intravenous NAL rapidly reversed all remi-induced effects. In a separate group of dogs, microinjections of DAMGO in the pre-BötC increased f(B) by 44%, while subsequent intravenous remi infusion more than offset this DAMGO induced tachypnea. These results indicate that mu-opioids at plasma concentrations that cause profound analgesia produce their bradypneic effect via MORs located outside the pre-BötC region.
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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.