ReviewCurrent opinion in pharmacology2016
Activity-triggered tetrapartite neuron-glial interactions following peripheral injury.
Review in Current opinion in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed.
- Peripheral and central pathogenesis of postherpetic neuralgia.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Review
- Glial Glutamate Transporter Modulation Prevents Development of Complete Freund's Adjuvant-Induced Hyperalgesia and Allodynia in Mice.Brain sciences · 2023Article
- Revolutionizing orofacial pain management: the promising potential of stem cell therapy.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- A novel cell-free intrathecal approach with PRP for the treatment of spinal cord multiple sclerosis in cats.Inflammation and regeneration · 2022Article
- Neuroimmune signatures in chronic low back pain subtypes.Brain : a journal of neurology · 2022Article
- Persistent, neuropathic-like trigeminal pain after dental implant loading.Journal of clinical and experimental dentistry · 2022Article
- The neuroinflammatory component of negative affect in patients with chronic pain.Molecular psychiatry · 2021Article
- Intravenous lidocaine alleviates postherpetic neuralgia in rats via regulation of neuroinflammation of microglia and astrocytes.iScience · 2021Article
- Bromelain reduced pro-inflammatory mediators as a common pathway that mediate antinociceptive and anti-anxiety effects in sciatic nerve ligated Wistar rats.Scientific reports · 2021Article
- Satellite Glial Cells in Pain Research: A Targeted Viewpoint of Potential and Future Directions.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- Modulatory Effects of Autophagy on APP Processing as a Potential Treatment Target for Alzheimer's Disease.Biomedicines · 2020Review
- Loss of SNHG4 Attenuated Spinal Nerve Ligation-Triggered Neuropathic Pain through Sponging miR-423-5p.Mediators of inflammation · 2020Article
- Sex-Dependent Glial Signaling in Pathological Pain: Distinct Roles of Spinal Microglia and Astrocytes.Neuroscience bulletin · 2018Article
- Neuropeptides and ATP signaling in the trigeminal ganglion.The Japanese dental science review · 2017Review
- Basic/Translational Development of Forthcoming Opioid- and Nonopioid-Targeted Pain Therapeutics.Anesthesia and analgesia · 2017Review
- In vivo immune interactions of multipotent stromal cells underlie their long-lasting pain-relieving effect.Scientific reports · 2017Article
- EZH2 regulates spinal neuroinflammation in rats with neuropathic pain.Neuroscience · 2017Article
- Chronic pain and impaired glial glutamate transporter function in lupus-prone mice are ameliorated by blocking macrophage colony-stimulating factor-1 receptors.Journal of neurochemistry · 2017Article
- The impact of inflammation on respiratory plasticity.Experimental neurology · 2017Review
- Neuroprotective Effects of Exercise Treatments After Injury: The Dual Role of Neurotrophic Factors.Current neuropharmacology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Recent studies continue to support the proposition that non-neuronal components of the nervous system, mainly glial cells and associated chemical mediators, contribute to the development of neuronal hyperexcitability that underlies persistent pain conditions. In the event of peripheral injury, enhanced or abnormal nerve input is likely the most efficient way to activate simultaneously central neurons and glia. Injury induces phenotypic changes in glia and triggers signaling cascades that engage reciprocal interactions between presynaptic terminals, postsynaptic neurons, microglia and astrocytes. While some responses to peripheral injury may help the nervous system to adapt positively to counter the disastrous effect of injury, the net effect often leads to long-lasting sensitization of pain transmission pathways and chronic pain.
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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.