ArticlePloS one2012
Comparative pharmacology of cholecystokinin induced activation of cultured vagal afferent neurons from rats and mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Cholecystokinin Induces CaThe European journal of neuroscience · 2026Article
- Comparison of receptor expression and cholecystokinin signaling between left and right nodose ganglia.American journal of physiology. Cell physiology · 2026Article
- Cholecystokinin receptor expression and signaling remain constant across time of day in rat vagal afferent neurons.American journal of physiology. Cell physiology · 2025Article
- 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
- TRPM3 expression and control of glutamate release from primary vagal afferent neurons.Journal of neurophysiology · 2021Article
- Cannabidiol activation of vagal afferent neurons requires TRPA1.Journal of neurophysiology · 2020Article
- Contributing mechanisms underlying desensitization of cholecystokinin-induced activation of primary nodose ganglia neurons.American journal of physiology. Cell physiology · 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
- 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
- Ethyl Vanillin Activates TRPA1.The Journal of pharmacology and experimental therapeutics · 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
- Inhibitory effects of capsaicin on voltage-gated potassium channels by TRPV1-independent pathway.Cellular and molecular neurobiology · 2014Article
- Subtype identification in acutely dissociated rat nodose ganglion neurons based on morphologic parameters.International journal of biological sciences · 2013Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
Cholecystokinin (CCK) facilitates the process of satiation via activation of vagal afferent neurons innervating the upper gastrointestinal tract. Recent findings indicate CCK acts on these neurons via a ruthenium red (RuR) sensitive pathway that involves members of the vanilloid (V) subfamily of transient receptor potential (TRP) channels. To further test this mechanism, the mouse provides an ideal model in which genetic tools could be applied. However, whether CCK acts by similar mechanism(s) in mice has not been determined. In the present study we explored the actions of CCK on nodose neurons isolated from Sprague Dawley (SD) rat and two strains of mice; C57BL/6 and BalbC using fluorescence-based calcium imaging. With minor exceptions nodose neurons isolated from all species/strains behaved similarly. They all respond to brief depolarization with a large calcium transient. A significant subset of neurons responded to capsaicin (CAP), a TRPV1 agonist, although neurons from C57BL/6 were 10-fold more sensitive to CAP than SD rats or BalbC mice, and a significantly smaller fraction of neurons from BalbC mice responded to CAP. CCK-8 dose-dependently activated a subpopulation of neurons with similar dose dependency, percent responders, and overlap between CCK and CAP responsiveness. In all species/strains CCK-8 induced activation was significantly attenuated (but not completely blocked) by pretreatment with the TRPV channel blocker RuR. Surprisingly, the CCK analogue JMV-180, which is reported to have pure antagonistic properties in rat but mixed agonist/antagonist properties in mice, behaved as a pure antagonist to CCK in both rat and mouse neurons. The pure antagonistic action of JMV-180 in this in vitro preparation suggests that prior reported differential effects of JMV-180 on satiation in rats versus mouse must be mediated by a site other than vagal afferent activation.
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Registered trials
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