ArticlePhysiological reports2018
Activity in nodose ganglia neurons after treatment with CP 55,940 and cholecystokinin.
Article in Physiological reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed.
- A distinct vagus-beta cell neural circuit senses glucose and modulates insulin secretion.Molecular metabolism · 2026Article
- Non-neuronal crosstalk promotes an inflammatory response in nodose ganglia cultures after exposure to byproducts from gram positive, high-fat-diet-associated gut bacteria.Physiology & behavior · 2020Article
- Gastrointestinal dysfunction after spinal cord injury.Experimental neurology · 2019Review
- Activity in nodose ganglia neurons after treatment with CP 55,940 and cholecystokinin.Physiological reports · 2018Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous work has shown that cannabinoids increase feeding, while cholecystokinin (CCK) has an anorexigenic effect on food intake. Receptors for these hormones are located on cell bodies of vagal afferent nerves in the nodose ganglia. An interaction between CCK and endocannabinoid receptors has been suggested. The purpose of these studies is to explore the effect of pretreatment with a cannabinoid agonist, CP 55,940, on nodose neuron activation by CCK. To determine the effect of CP 55,940 and CCK on neuron activation, rats were anesthetized and nodose ganglia were excised. The neurons were dissociated and placed in culture on coverslips. The cells were treated with media; CP 55,940; CCK; CP 55,940 followed by CCK; or AM 251, a CB1 receptor antagonist, and CP 55,940 followed by CCK. Immunohistochemistry was performed to stain the cells for cFos as a measure of cell activation. Neurons were identified using neurofilament immunoreactivity. The neurons on each slip were counted using fluorescence imaging, and the number of neurons that were cFos positive was counted in order to calculate the percentage of activated neurons per coverslip. Pretreatment with CP 55,940 decreased the percentage of neurons expressing cFos-immunoreactivity in response to CCK. This observation suggests that cannabinoids inhibit CCK activation of nodose ganglion neurons.
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