ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Allergic inflammation in isolated vagal sensory ganglia unmasks silent NK-2 tachykinin receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 50 citations in OpenAlex.
- Inhibitory neurotransmission regulates vagal efferent activity and gastric motility.Experimental biology and medicine (Maywood, N.J.) · 2016Review
- Quantitative Magnetization Transfer Imaging as a Biomarker for Effects of Systemic Inflammation on the Brain.Biological psychiatry · 2015Article
- Role of central vagal 5-HT3 receptors in gastrointestinal physiology and pathophysiology.Frontiers in neuroscience · 2015Review
- Neurogenic airway inflammation induced by repeated intra-esophageal instillation of HCl in guinea pigs.Inflammation · 2013Article
- Three days after a single exposure to ozone, the mechanism of airway hyperreactivity is dependent on substance P and nerve growth factor.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Central nervous system neurons acquire mast cell products via transgranulation.The European journal of neuroscience · 2005Article
- Substance P-mediated modulation of pacemaker properties in the mammalian respiratory network.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Calcium and calcium-activated currents in vagotomized rat primary vagal afferent neurons.The Journal of physiology · 2002Article
- Neurokinin B- and specific tachykinin NK(3) receptor agonists-induced airway hyperresponsiveness in the guinea-pig.British journal of pharmacology · 2000Article
- Role of tachykinin NK2 receptors in normal and altered rectal sensitivity in rats.British journal of pharmacology · 2000Article
- Mast cells migrate from blood to brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Calcium regulation of a slow post-spike hyperpolarization in vagal afferent neurons.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Serotonin unmasks functional NK-2 receptors in vagal sensory neurones of the guinea-pig.The Journal of physiology · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neuroplastic changes in vagal afferents inflicted by allergic inflammation were examined in nodose ganglia (NG) removed from guinea pigs immunized to chick ovalbumin. In control NG neurons, substance P (SP; 0.1-10 microM) produces no discernable changes in membrane electrophysiological properties or [Ca2+]i. After exposing NG from immunized animals to the sensitizing antigen in vitro, 83% of the neurons were depolarized by 100 nM SP. SP also produces an inward current, an increase in membrane conductance, and an elevation of [Ca2+]i. Buffering [Ca2+]i with BAPTA blocked the [Ca2+]i rise and the SP depolarization, indicating that internal stores of Ca2+ are required. When protein synthesis was inhibited >96% (as determined by [3H] leucine incorporation), antigen challenge still unmasked SP responses. The SP response was maximal 30 min after antigen challenge, and it was evident for at least 8 hr in intact ganglia and for 3.5 d in isolated neurons. [beta-Ala8]Neurokinin A ([beta-Ala8]NKA; 10 nM), an NK-2 selective agonist, mimicked SP; selective NK-1 and NK-3 agonists were ineffective. The EC50 values for SP and [beta-Ala8]NKA membrane currents were 78 and 33 nM, respectively. Additionally, SR48968, an NK-2 receptor antagonist, blocked these responses. Thus, antigen challenge appears to unmask an NK-2 tachykinin receptor. These data further support the hypothesis that inflammatory mediators released during immediate hypersensitivity (allergic) reactions can produce profound effects on the excitability of sensory nerves. Unmasked NK-2 receptors may serve an excitatory autoreceptor function, provide a pathway for paracrine signaling between NG neurons, and contribute to ectopic sensory nerve activity.
Indexed as
Identifiers
9315890PMC6793896W2167087403What 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.