ArticlePain2008
Role of ASIC3 in the primary and secondary hyperalgesia produced by joint inflammation in mice.
Article in Pain, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 154 citations in OpenAlex.
- Acid-induced experimental knee pain and hyperalgesia in healthy humans.Experimental brain research · 2018Trial
- Acidic buffer induced muscle pain evokes referred pain and mechanical hyperalgesia in humans.Pain · 2008Trial
- PUFA modulation of ASIC3 involves both specific and lipid solvent-like interactions.bioRxiv : the preprint server for biology · 2026Article
- Expression of Acid-Sensing Ion Channel 3 in Afferents Averts Long-Term Sensitization and the Development of Visceral Pain.International journal of molecular sciences · 2024Article
- Complex alterations in inflammatory pain and analgesic sensitivity in young and ageing female rats: involvement of ASIC3 and Nav1.8 in primary sensory neurons.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- The role of acid-sensing ion channels in monosodium urate-induced gouty pain in mice.Pflugers Archiv : European journal of physiology · 2024Article
- Commentary: Effects of combined treatment with transcranial and peripheral electromagnetic stimulation on performance and pain recovery from delayed onset muscle soreness induced by eccentric exercise in young athletes. A randomized clinical trial.Frontiers in physiology · 2024Article
- Vacuolar-ATPase-mediated muscle acidification caused muscular mechanical nociceptive hypersensitivity after chronic stress in rats, which involved extracellular matrix proteoglycan and ASIC3.Scientific reports · 2023Article
- Regulation of pain neurotransmitters and chondrocytes metabolism mediated by voltage-gated ion channels: A narrative review.Heliyon · 2023Review
- Peripheral and central employment of acid-sensing ion channels during early bilaterian evolution.eLife · 2023Article
- Calcium-Permeable Channels Cooperation for Rheumatoid Arthritis: Therapeutic Opportunities.Biomolecules · 2022Review
- Should We Void Lactate in the Pathophysiology of Delayed Onset Muscle Soreness? Not So Fast! Let's See a Neurocentric View!Metabolites · 2022Article
- Osteoporosis in Light of a New Mechanism Theory of Delayed Onset Muscle Soreness and Non-Contact Anterior Cruciate Ligament Injury.International journal of molecular sciences · 2022Article
- Is the Sex Difference a Clue to the Pathomechanism of Dry Eye Disease? Watch out for the NGF-TrkA-Piezo2 Signaling Axis and the Piezo2 Channelopathy.Journal of molecular neuroscience : MN · 2022Review
- Pathology and physiology of acid‑sensitive ion channels in the digestive system (Review).International journal of molecular medicine · 2022Review
- Gut Mucosal Microbiome Is Perturbed in Rheumatoid Arthritis Mice and Partly Restored after TDAG8 Deficiency or Suppression by Salicylanilide Derivative.International journal of molecular sciences · 2022Article
- Acid-sensing ion channel 3: An analgesic target.Channels (Austin, Tex.) · 2021Review
- Finishing stationary cycling too early after anterior cruciate ligament reconstruction is likely to lead to higher failure.BMC sports science, medicine & rehabilitation · 2021Article
- Citric Acid in Drug Formulations Causes Pain by Potentiating Acid-Sensing Ion Channel 1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Inhibiting BDNF/TrkB.T1 receptor improves resiniferatoxin-induced postherpetic neuralgia through decreasing ASIC3 signaling in dorsal root ganglia.Journal of neuroinflammation · 2021Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The acid sensing ion channel 3 (ASIC3) is critical for the development of secondary hyperalgesia as measured by mechanical stimulation of the paw following muscle insult. We designed experiments to test whether ASIC3 was necessary for the development of both primary and secondary mechanical hyperalgesia that develops after joint inflammation. We used ASIC3 -/- mice and examined the primary (response to tweezers) and secondary hyperalgesia (von-Frey filaments) that develops after joint inflammation comparing to ASIC3 +/+ mice. We also examined the localization of ASIC3 to the knee joint afferents innervating the synovium using immunohistochemical techniques before and after joint inflammation. We show that secondary mechanical hyperalgesia does not develop in ASIC3 -/- mice. However, the primary mechanical hyperalgesia of the inflamed knee joint still develops in ASIC3 -/- mice and is similar to ASIC3 +/+ mice. In knee joint synovium from ASIC3 +/+ mice without joint inflammation, ASIC3 was not localized to joint afferents that were stained with an antibody to protein gene product (PGP) 9.5 or calcitonin gene-related peptide (CGRP). ASIC3 was found, however, in synoviocytes of the knee joint of uninflamed mice. In ASIC3 +/+ mice with joint inflammation, ASIC3 co-localized with PGP 9.5 or CGRP in joint afferents innervating the synovium. We conclude that the decreased pH that occurs after inflammation would activate ASIC3 on primary afferent fibers innervating the knee joint, increasing the input to the spinal cord resulting in central sensitization manifested behaviorally as secondary hyperalgesia of the paw.
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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.