ArticleNeurogastroenterology and motility2012
Glucose-dependent trafficking of 5-HT3 receptors in rat gastrointestinal vagal afferent neurons.
Article in Neurogastroenterology and motility, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Oestrogen modulates stress-induced vagally-dependent gastric responses to oxytocin.The Journal of physiology · 2026Article
- Article
- 5-HTInternational journal of molecular sciences · 2023Article
- The physiological control of eating: signals, neurons, and networks.Physiological reviews · 2022 · on this mapArticle
- Tapping into 5-HTInternational journal of molecular sciences · 2021Review
- Central Neurocircuits Regulating Food Intake in Response to Gut Inputs-Preclinical Evidence.Nutrients · 2021Review
- Structure, Function and Physiology of 5-Hydroxytryptamine Receptors Subtype 3.Sub-cellular biochemistry · 2021Review
- Blunted Vagal Cocaine- and Amphetamine-Regulated Transcript Promotes Hyperphagia and Weight Gain.Cell reports · 2020Article
- Stress-induced modulation of vagal afferents.Neurogastroenterology and motility · 2019Review
- The gut microbiota to the brain axis in the metabolic control.Reviews in endocrine & metabolic disorders · 2019Review
- Signalling from the periphery to the brain that regulates energy homeostasis.Nature reviews. Neuroscience · 2018Review
- 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
- Novel developments in vagal afferent nutrient sensing and its role in energy homeostasis.Current opinion in pharmacology · 2016Review
- What goes around comes around: novel pharmacological targets in the gut-brain axis.Therapeutic advances in gastroenterology · 2016Review
- High fat diet attenuates glucose-dependent facilitation of 5-HT3 -mediated responses in rat gastric vagal afferents.The Journal of physiology · 2016Article
- Macrophages in diabetic gastroparesis--the missing link?Neurogastroenterology and motility · 2015Review
- Role of central vagal 5-HT3 receptors in gastrointestinal physiology and pathophysiology.Frontiers in neuroscience · 2015Review
- Article
- Exposure to a high fat diet during the perinatal period alters vagal motoneurone excitability, even in the absence of obesity.The Journal of physiology · 2015Article
- Central nervous system control of gastrointestinal motility and secretion and modulation of gastrointestinal functions.Comprehensive Physiology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIntestinal glucose induces gastric relaxation via vagally mediated sensory-motor reflexes. Glucose can alter the activity of gastrointestinal (GI) vagal afferent (sensory) neurons directly, via closure of ATP-sensitive potassium channels, and indirectly, via the release of 5-hydroxytryptamine (5-HT) from mucosal enteroendocrine cells. We hypothesized that glucose may also be able to modulate the ability of GI vagal afferent neurons to respond to the released 5-HT, via regulation of neuronal 5-HT(3) receptors.
methodsWhole-cell patch clamp recordings were made from acutely dissociated GI-projecting vagal afferent neurons exposed to equiosmolar Krebs' solution containing different concentrations of d-glucose (1.25-20 mmol L(-1)) and the response to picospritz application of 5-HT assessed. The distribution of 5-HT(3) receptors in neurons exposed to different glucose concentrations was also assessed immunohistochemically. KEY
resultsIncreasing or decreasing extracellular d-glucose concentration increased or decreased, respectively, the 5-HT-induced inward current and the proportion of 5-HT(3) receptors associated with the neuronal membrane. These responses were blocked by the Golgi-disrupting agent Brefeldin-A (5 μmol L(-1)) suggesting involvement of a protein-trafficking pathway. Furthermore, l-glucose did not mimic the response of d-glucose implying that metabolic events downstream of neuronal glucose uptake are required to observe the modulation of 5-HT(3) receptor mediated responses. CONCLUSIONS & INFERENCES: These results suggest that, in addition to inducing the release of 5-HT from enterochromaffin cells, glucose may also increase the ability of GI vagal sensory neurons to respond to the released 5-HT, providing a means by which the vagal afferent signal can be amplified or prolonged.
Indexed as
Identifiers
What OpenQuestion holds
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.