ArticleJournal of neurophysiology2020
Loss of excitatory amino acid transporter restraint following chronic intermittent hypoxia contributes to synaptic alterations in nucleus tractus solitarii.
Article in Journal of neurophysiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 16 citations in OpenAlex.
- Quantitative and morphological analyses reveal microglia-specific neuroinflammation in brain regions linked to cognitive function in ovariectomized and chronic intermittent hypoxia-exposed female rats.Brain, behavior, & immunity - health · 2026Article
- The development but not the maintenance of phrenic and sympathetic long-term facilitation after acute intermittent hypoxia requires nucleus tractus solitarii HExperimental neurology · 2025Article
- Reactive Oxidative Species in Carotid Body Chemoreception: Their Role in Oxygen Sensing and Cardiorespiratory Alterations Induced by Chronic Intermittent Hypoxia.Antioxidants (Basel, Switzerland) · 2025Review
- Oxytocin and corticotropin-releasing hormone exaggerate nucleus tractus solitarii neuronal and synaptic activity following chronic intermittent hypoxia.The Journal of physiology · 2024Article
- Vagotomy blunts cardiorespiratory responses to vagal afferent stimulation via pre- and postsynaptic effects in the nucleus tractus solitarii.The Journal of physiology · 2024Article
- Circadian disruptions and their role in the development of hypertension.Frontiers in neuroscience · 2024Review
- Nucleus tractus solitarii is required for the development and maintenance of phrenic and sympathetic long-term facilitation after acute intermittent hypoxia.Frontiers in physiology · 2023Article
- Chronic intermittent hypoxia enhances glycinergic inhibition in nucleus tractus solitarius.Journal of neurophysiology · 2022Article
- Glial Modulation of Energy Balance: The Dorsal Vagal Complex Is No Exception.International journal of molecular sciences · 2022Review
- Unilateral vagotomy alters astrocyte and microglial morphology in the nucleus tractus solitarii of the rat.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- The role of astrocytes in the nucleus tractus solitarii in maintaining central control of autonomic function.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Review
- Gamma-Aminobutyric Acid Transporters in the Nucleus Tractus Solitarii Regulate Inhibitory and Excitatory Synaptic Currents That Influence Cardiorespiratory Function.Frontiers in physiology · 2021Article
- Exaggerated potassium current reduction by oxytocin in visceral sensory neurons following chronic intermittent hypoxia.Autonomic neuroscience : basic & clinical · 2020Article
- Mechanisms Underlying Neuroplasticity in the Nucleus Tractus Solitarii Following Hindlimb Unloading in Rats.Neuroscience · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Peripheral viscerosensory afferent signals are transmitted to the nucleus tractus solitarii (nTS) via release of glutamate. Following release, glutamate is removed from the extrasynaptic and synaptic cleft via excitatory amino acid transporters (EAATs), thus limiting glutamate receptor activation or over activation, and maintaining its working range. We have shown that EAAT block with the antagonist
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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.