ArticleEndocrinology2010
Role of transient receptor potential channels in cholecystokinin-induced activation of cultured vagal afferent neurons.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Cholecystokinin receptor expression and signaling remain constant across time of day in rat vagal afferent neurons.American journal of physiology. Cell physiology · 2025Article
- Comparative analysis of the hypothalamus transcriptome of laying ducks with different residual feeding intake.Poultry science · 2024Article
- TRPV1 enhances cholecystokinin signaling in primary vagal afferent neurons and mediates the central effects on spontaneous glutamate release in the NTS.American journal of physiology. Cell physiology · 2024Article
- Hypoxia augments TRPM3-mediated calcium influx in vagal sensory neurons.Autonomic neuroscience : basic & clinical · 2023Article
- Role of Ion Channels in the Chemotransduction and Mechanotransduction in Digestive Function and Feeding Behavior.International journal of molecular sciences · 2022Review
- Estrogen and gut satiety hormones in vagus-hindbrain axis.Peptides · 2020Review
- Contributing mechanisms underlying desensitization of cholecystokinin-induced activation of primary nodose ganglia neurons.American journal of physiology. Cell physiology · 2020Article
- Early oral nutrition improves postoperative ileus through the TRPA1/CCK1-R-mediated mast cell-nerve axis.Annals of translational medicine · 2020Article
- Gastric vagal afferent neuropathy following experimental spinal cord injury.Experimental neurology · 2020Article
- TMEM16B determines cholecystokinin sensitivity of intestinal vagal afferents of nodose neurons.JCI insight · 2019Article
- TRPC6 in simulated microgravity of intervertebral disc cells.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2018Article
- Loss of Vagal Sensitivity to Cholecystokinin in Rats Born with Intrauterine Growth Retardation and Consequence on Food Intake.Frontiers in endocrinology · 2017Article
- Genetic and pharmacological evidence for low-abundance TRPV3 expression in primary vagal afferent neurons.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Mercaptoacetate blocks fatty acid-induced GLP-1 secretion in male rats by directly antagonizing GPR40 fatty acid receptors.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Leptin-induced spine formation requires TrpC channels and the CaM kinase cascade in the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Mercaptoacetate and fatty acids exert direct and antagonistic effects on nodose neurons via GPR40 fatty acid receptors.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Article
- Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.PloS one · 2012Article
- Pharmacological investigations of the cellular transduction pathways used by cholecystokinin to activate nodose neurons.Autonomic neuroscience : basic & clinical · 2011Article
- Transient receptor potential (TRP) channels as drug targets for diseases of the digestive system.Pharmacology & therapeutics · 2011Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cholecystokinin (CCK), an endogenous brain-gut peptide, is released after food intake and promotes the process of satiation via activation of the vagus nerve. In vitro, CCK increases cytosolic calcium concentrations and produces membrane depolarization in a subpopulation of vagal afferent neurons. However, the specific mechanisms and ionic conductances that mediate these effects remain unclear. In this study we used calcium imaging, electrophysiological measurements, and single cell PCR analysis on cultured vagal afferent neurons to address this issue directly. A cocktail of blockers of voltage-dependent calcium channels (VDCC) failed to block CCK-induced calcium responses. In addition, SKF96365, a compound that blocks both VDCC and the C family of transient receptor potential (TRP) channels, also failed to prevent responses to CCK. Together these results suggest that CCK-induced calcium influx is not subsequent to the membrane depolarization. Ruthenium red, an inhibitor of the TRPV family and TRPA1, blocked both depolarizing responses to CCK and CCK-induced calcium increases, but had no effect on the KCl-induced calcium response. Selective block of TRPV1 and TRPA1 channels with SB366791 and HC030031, respectively, had minor effects on the CCK-induced response. Application of 2-aminoethoxydiphenyl borate, an activator of select TRPV channels but a blocker of several TRPC channels, either had no effect or enhanced the responses to CCK. Further, results from PCR experiments revealed a significant clustering of TRPV2-5 in neurons expressing CCK1 receptors. These observations demonstrate that CCK-induced increases in cytosolic calcium and membrane depolarization of vagal afferent neurons are likely mediated by TRPV channels, excluding TRPV1.
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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.