ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Tumor necrosis factor activation of vagal afferent terminal calcium is blocked by cannabinoids.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 19 citations in OpenAlex.
- Mechanisms of Nausea and Vomiting: Current Knowledge and Recent Advances in Intracellular Emetic Signaling Systems.International journal of molecular sciences · 2021Review
- Peripheral-to-central immune communication at the area postrema glial-barrier following bleomycin-induced sterile lung injury in adult rats.Brain, behavior, and immunity · 2020Article
- Dorsal vagal complex and hypothalamic glia differentially respond to leptin and energy balance dysregulation.Translational psychiatry · 2020Article
- Evidence that hindbrain astrocytes in the rat detect low glucose with a glucose transporter 2-phospholipase C-calcium release mechanism.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Selective Targeting of TNF Receptors as a Novel Therapeutic Approach.Frontiers in cell and developmental biology · 2020Review
- Response of catecholaminergic neurons in the mouse hindbrain to glucoprivic stimuli is astrocyte dependent.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Lung-injury depresses glutamatergic synaptic transmission in the nucleus tractus solitarii via discrete age-dependent mechanisms in neonatal rats.Brain, behavior, and immunity · 2018Article
- Visceral Inflammation and Immune Activation Stress the Brain.Frontiers in immunology · 2017Review
- Divergent neuroendocrine responses to localized and systemic inflammation.Seminars in immunology · 2014Review
- Endocannabinoids blunt the augmentation of synaptic transmission by serotonin 2A receptors in the nucleus tractus solitarii (nTS).Brain research · 2013Article
- Anandamide, cannabinoid type 1 receptor, and NMDA receptor activation mediate non-Hebbian presynaptically expressed long-term depression at the first central synapse for visceral afferent fibers.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Astrocytes in the nucleus of the solitary tract are activated by low glucose or glucoprivation: evidence for glial involvement in glucose homeostasis.Frontiers in neuroscience · 2013Article
- St. John's Wort enhances the synaptic activity of the nucleus of the solitary tract.Nutrition (Burbank, Los Angeles County, Calif.)Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The early proinflammatory cytokine tumor necrosis factor (TNF) is released in significant quantities by the activated immune system in response to infection, leukemia, autoimmune disorders, and radiation sickness. Nausea, emesis, and anorexia are common features of these disorders. TNF action on vagal afferent terminals in the brainstem is a likely cause of the malaise associated with these disorders. Our previous work has shown that TNF action to excite vagal afferents occurs as a result of sensitization of ryanodine channels in afferent nerve terminals. For millennia, cannabinoids (CB) have been used to combat the visceral malaise associated with chronic disease, although the mechanism of action has not been clear. Previous work in culture systems suggests that CB1 agonists can suppress neurotransmission by downregulating ryanodine channels through a protein kinase A (PKA)-dependent mechanism. Laser confocal calcium imaging methods were used to directly examine effects of CB1 cannabinoid agonists and TNF on visceral afferent signaling in the rat hindbrain. CB1 agonists blocked the effects of TNF to amplify vagal afferent responsiveness; blockade of PKA with H89 also eliminated the TNF amplification effect. These results help to explain the effectiveness of cannabinoids in blocking the malaise generated by TNF-releasing disease processes by opposing effects on ryanodine channels.
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Registered trials
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