ArticleThe Journal of physiology2009
Activation of the retrotrapezoid nucleus by posterior hypothalamic stimulation.
Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 61 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
- Interactions between Arousal State and COThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Intrinsic Molecular Proton Sensitivity Underlies GPR4 Effects on Retrotrapezoid Nucleus Neuronal Activation and COThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Article
- Central respiratory chemoreception.Handbook of clinical neurology · 2022Review
- Carotid bodies contribute to sympathoexcitation induced by acute salt overload.Experimental physiology · 2019Article
- Bilateral carotid sinus nerve transection exacerbates morphine-induced respiratory depression.European journal of pharmacology · 2018Article
- Impaired central respiratory chemoreflex in an experimental genetic model of epilepsy.The Journal of physiology · 2017Article
- The effects of slow-paced versus mechanically assisted breathing on autonomic function in fibromyalgia patients.Journal of pain research · 2017Article
- Sciatic nerve stimulation activates the retrotrapezoid nucleus in anesthetized rats.Journal of neurophysiology · 2016Article
- Respiratory and autonomic dysfunction in congenital central hypoventilation syndrome.Journal of neurophysiology · 2016Review
- Proton detection and breathing regulation by the retrotrapezoid nucleus.The Journal of physiology · 2016Review
- Facilitation of breathing by leptin effects in the central nervous system.The Journal of physiology · 2016Review
- PHYSIOLOGY. Regulation of breathing by CO₂ requires the proton-activated receptor GPR4 in retrotrapezoid nucleus neurons.Science (New York, N.Y.) · 2015Article
- Activation of the brain melanocortin system is required for leptin-induced modulation of chemorespiratory function.Acta physiologica (Oxford, England) · 2015Article
- Control of respiratory and cardiovascular functions by leptin.Life sciences · 2015Review
- Hypoxia silences retrotrapezoid nucleus respiratory chemoreceptors via alkalosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Regulation of breathing and autonomic outflows by chemoreceptors.Comprehensive Physiology · 2014Review
- Autonomic deficit not the cause of death in West Nile virus neurological disease.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2014Article
- Chemoreception and asphyxia-induced arousal.Respiratory physiology & neurobiology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The retrotrapezoid nucleus (RTN) contains chemically defined neurons (ccRTN neurons) that provide a pH-regulated excitatory drive to the central respiratory pattern generator. Here we test whether ccRTN neurons respond to stimulation of the perifornical hypothalamus (PeF), a region that regulates breathing during sleep, stress and exercise. PeF stimulation with gabazine increased blood pressure, phrenic nerve discharge (PND) and the firing rate of ccRTN neurons in isoflurane-anaesthetized rats. Gabazine produced an approximately parallel upward shift of the steady-state relationship between ccRTN neuron firing rate and end-tidal CO(2), and a similar shift of the relationship between PND and end-tidal CO(2). The central respiratory modulation of ccRTN neurons persisted after gabazine without a change in pattern. Morphine administration typically abolished PND and reduced the discharge rate of most ccRTN neurons (by 25% on average). After morphine administration, PeF stimulation activated the ccRTN neurons normally but PND activation and the central respiratory modulation of the ccRTN neurons were severely attenuated. In the same rat preparation, most (58%) ccRTN neurons expressed c-Fos after exposure to hypercapnic hyperoxia (6-7% end-tidal CO(2); 3.5 h; no hypothalamic stimulation) and 62% expressed c-Fos under hypocapnia (approximately 3% end-tidal CO(2)) after PeF stimulation. Under baseline conditions (approximately 3% end-tidal CO(2), hyperoxia, no PeF stimulation) few (11%) ccRTN neurons expressed c-Fos. In summary, most ccRTN neurons are excited by posterior hypothalamic stimulation while retaining their normal response to CNS acidification. ccRTN neurons probably contribute both to the chemical drive of breathing and to the feed-forward control of breathing associated with emotions and or locomotion.
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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.