ArticleProceedings of the National Academy of Sciences of the United States of America2012
An antinociceptive role for substance P in acid-induced chronic muscle pain.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 97 citations in OpenAlex.
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- Effect of acupuncture on pain and substance P levels in middle-aged women with chronic neck pain.Frontiers in neurology · 2023Article
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- Bioactive Compounds for Fibromyalgia-like Symptoms: A Narrative Review and Future Perspectives.International journal of environmental research and public health · 2022Review
- Novel Pituitary Actions of TAC4 Gene Products in Teleost.International journal of molecular sciences · 2021Article
- Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update.International journal of molecular sciences · 2021Review
- Activation of acid-sensing ion channel 3 by lysophosphatidylcholine 16:0 mediates psychological stress-induced fibromyalgia-like pain.Annals of the rheumatic diseases · 2020Article
Corrections and comments
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Authors and funding
6 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Release of substance P (SP) from nociceptive nerve fibers and activation of its receptor neurokinin 1 (NK1) are important effectors in the transmission of pain signals. Nonetheless, the role of SP in muscle pain remains unknown. Here we show that a single i.m. acid injection in mice lacking SP signaling by deletion of the tachykinin precursor 1 (Tac1) gene or coadministration of NK1 receptor antagonists produces long-lasting hyperalgesia rather than the transient hyperalgesia seen in control animals. The inhibitory effect of SP was found exclusively in neurons expressing acid-sensing ion channel 3, where SP enhances M-channel-like potassium currents through the NK1 receptor in a G protein-independent but tyrosine kinase-dependent manner. Furthermore, the SP signaling could alter action potential thresholds and modulate the expression of TTX-resistant sodium currents in medium-sized muscle nociceptors. Thus, i.m. SP mediates an unconventional NK1 receptor signal pathway to inhibit acid activation in muscle nociceptors, resulting in an unexpected antinociceptive effect against chronic mechanical hyperalgesia, here induced by repeated i.m. acid injection.
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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.