ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Nerve growth factor sensitizes adult sympathetic neurons to the proinflammatory peptide bradykinin.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Kallikrein-kinin system as a potential target for the treatment of intervertebral disc degeneration.European journal of medical research · 2025Review
- Sympathetic motor neuron dysfunction is a missing link in age-associated sympathetic overactivity.eLife · 2024Article
- Sympathetic Motor Neuron Dysfunction is a Missing Link in Age-Associated Sympathetic Overactivity.bioRxiv : the preprint server for biology · 2024Article
- Expression of glucagon-like peptide 1 receptor in neuropeptide Y neurons of the arcuate nucleus in mice.Brain structure & function · 2022Article
- Structural and Functional Coupling of Calcium-Activated BK Channels and Calcium-Permeable Channels Within Nanodomain Signaling Complexes.Frontiers in physiology · 2021Review
- Control of Neuronal Excitability by Cell Surface Receptor Density and Phosphoinositide Metabolism.Frontiers in pharmacology · 2021Article
- Understanding phosphoinositides: rare, dynamic, and essential membrane phospholipids.The Biochemical journal · 2019Review
- Recent advances in understanding phosphoinositide signaling in the nervous system.F1000Research · 2019Review
- Proximal clustering between BK and CaeLife · 2017Article
- Possible Reversal of PTSD-Related DNA Methylation by Sympathetic Blockade.Journal of molecular neuroscience : MN · 2017Review
- Immunological Mechanisms Underlying Chronic Pelvic Pain and Prostate Inflammation in Chronic Pelvic Pain Syndrome.Frontiers in immunology · 2017Review
- Mechanisms of nerve growth factor signaling in bone nociceptors and in an animal model of inflammatory bone pain.Molecular pain · 2017Article
- Electrophysiological Investigation of the Subcellular Fine Tuning of Sympathetic Neurons by Hydrogen Sulfide.Frontiers in pharmacology · 2017Article
- Osmoregulatory inositol transporter SMIT1 modulates electrical activity by adjusting PI(4,5)P2 levels.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Dynamic formation of ER-PM junctions presents a lipid phosphatase to regulate phosphoinositides.The Journal of cell biology · 2016Article
- Ciliary neurotrophic factor-treated astrocyte-conditioned medium increases the intracellular free calcium concentration in rat cortical neurons.Biomedical reports · 2016Article
- Molecular Mechanisms of Sympathetic Remodeling and Arrhythmias.Circulation. Arrhythmia and electrophysiology · 2016Review
- Dynamics of Phosphoinositide-Dependent Signaling in Sympathetic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
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3 authors.
Funding
Abstract
Levels of nerve growth factor (NGF) are elevated in inflamed tissues. In sensory neurons, increases in NGF augment neuronal sensitivity (sensitization) to noxious stimuli. Here, we hypothesized that NGF also sensitizes sympathetic neurons to proinflammatory stimuli. We cultured superior cervical ganglion (SCG) neurons from adult male Sprague Dawley rats with or without added NGF and compared their responsiveness to bradykinin, a proinflammatory peptide. The NGF-cultured neurons exhibited significant depolarization, bursts of action potentials, and Ca(2+) elevations after bradykinin application, whereas neurons cultured without NGF showed only slight changes in membrane potential and cytoplasmic Ca(2+) levels. The NGF effect, which requires trkA receptors, takes hours to develop and days to reverse. We addressed the ionic mechanisms underlying this sensitization. NGF did not alter bradykinin-induced M-current inhibition or phosphatidylinositol 4,5-bisphosphate hydrolysis. Maxi-K channel-mediated current evoked by depolarizations was reduced by 50% by culturing neurons in NGF. Application of iberiotoxin or paxilline, blockers of Maxi-K channels, mimicked NGF treatment and sensitized neurons to bradykinin application. A calcium channel blocker also mimicked NGF treatment. We found that NGF reduces Maxi-K channel opening by decreasing the activity of nifedipine-sensitive calcium channels. In conclusion, culture in NGF reduces the activity of L-type calcium channels, and secondarily, the calcium-sensitive activity of Maxi-K channels, rendering sympathetic neurons electrically hyper-responsive to bradykinin.
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