ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2008
Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT3 receptors.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Insulin level regulators may affect cognitive ability caused by motion sickness: an experimental study.Metabolic brain disease · 2025Article
- Plasma Concentrations of Oral Ondansetron in Hospitalized Dogs Exhibiting Clinical Signs of Nausea.Veterinary sciences · 2024Article
- Systemic Glucose Regulation by a Hindbrain Inhibitory Circuit in a Mouse Model of Type 1 Diabetes.Neuroendocrinology · 2024Article
- Gut liver brain axis in diseases: the implications for therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- 5-HTInternational journal of molecular sciences · 2023Article
- DMV extrasynaptic NMDA receptors regulate caloric intake in rats.JCI insight · 2021Article
- Glutamatergic plasticity within neurocircuits of the dorsal vagal complex and the regulation of gastric functions.American journal of physiology. Gastrointestinal and liver physiology · 2021Review
- Central Neurocircuits Regulating Food Intake in Response to Gut Inputs-Preclinical Evidence.Nutrients · 2021Review
- Ethanol induces persistent potentiation of 5-HTNeuropharmacology · 2021Article
- Structure, Function and Physiology of 5-Hydroxytryptamine Receptors Subtype 3.Sub-cellular biochemistry · 2021Review
- Musings on the wanderer: What's new in our understanding of vago-vagal reflexes? VI. Central vagal circuits that control glucose metabolism.American journal of physiology. Gastrointestinal and liver physiology · 2021Review
- Cellular and systemic mechanisms for glucose sensing and homeostasis.Pflugers Archiv : European journal of physiology · 2020Review
- High glucose increases action potential firing of catecholamine neurons in the nucleus of the solitary tract by increasing spontaneous glutamate inputs.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Plasticity of vagal afferent signaling in the gut.Medicina (Kaunas, Lithuania) · 2017Review
- Microbiome-Gut-Brain Axis: A Pathway for Improving Brainstem Serotonin Homeostasis and Successful Autoresuscitation in SIDS-A Novel Hypothesis.Frontiers in pediatrics · 2016Article
- Glycemic state regulates melanocortin, but not nesfatin-1, responsiveness of glucose-sensing neurons in the nucleus of the solitary tract.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Cardiovascular afferents cause the release of 5-HT in the nucleus tractus solitarii; this release is regulated by the low- (PMAT) not the high-affinity transporter (SERT).The Journal of physiology · 2015Article
- Role of central vagal 5-HT3 receptors in gastrointestinal physiology and pathophysiology.Frontiers in neuroscience · 2015Review
- Central nervous system control of gastrointestinal motility and secretion and modulation of gastrointestinal functions.Comprehensive Physiology · 2014Review
- Modulation of gastrointestinal vagal neurocircuits by hyperglycemia.Frontiers in neuroscience · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Acute hyperglycemia has profound effects on vagally mediated gastrointestinal functions. We have reported recently that the release of glutamate from the central terminals of vagal afferent neurons is correlated directly with the extracellular glucose concentration. The present study was designed to test the hypothesis that 5-HT(3) receptors present on vagal afferent nerve terminals are involved in this glucose-dependent modulation of glutamatergic synaptic transmission. Whole-cell patch-clamp recordings were made from neurons of the nucleus tractus solitarius (NTS) in thin rat brainstem slices. Spontaneous and evoked glutamate release was decreased in a concentration-dependent manner by the 5-HT(3) receptor selective antagonist, ondansetron. Alterations in the extracellular glucose concentration induced parallel shifts in the ondansetron-mediated inhibition of glutamate release. The changes in excitatory synaptic transmission induced by extracellular glucose concentration were mimicked by the serotonin uptake inhibitor, fenfluramine. These data suggest that glucose alters excitatory synaptic transmission within the rat brainstem via actions on tonically active 5-HT(3) receptors, and the number of 5-HT(3) receptors on vagal afferent nerve terminals is positively correlated with the extracellular glucose concentration. These data indicate that the 5-HT(3) receptors present on synaptic connections between vagal afferent nerve terminals and NTS neurons are a strong candidate for consideration as one of the sites where glucose acts to modulate vagovagal reflexes.
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