ArticlePharmaceuticals (Basel, Switzerland)2022
Segmental Upregulation of ASIC1 Channels in the Formalin Acute Pain Mouse Model.
Article in Pharmaceuticals (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- The analgesic effect and mechanism of celastrol in formalin-induced inflammatory pain mouse model.Molecular and cellular biochemistry · 2026Article
- Two Amino Acid Substitutions Improve the Pharmacological Profile of the Snake Venom Peptide Mambalgin.Toxins · 2025Article
- ASIC1a-associated mechanical hypersensitivity in the GlaKO Fabry disease mouse model.Neurobiology of pain (Cambridge, Mass.)Article
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9 authors at 1 institution in 1 country.
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Abstract
backgroundHindpaw injection of formalin in rodents is used to assess acute persistent pain. The response to formalin is biphasic. The initial response (first minutes) is thought to be linked to inflammatory, peripheral mechanisms, while the latter (around 30 min after the injection), is linked to central mechanisms. This model is useful to analyze the effect of drugs at one or both phases, and the involvement of ion channels in the response. Acid-sensing ion channels (ASICs) regulate synaptic activities and play important roles in pain conditions. Recently, psalmotoxin-1 (Pctx-1), a toxin that inhibits ASIC1a-constituted channels, and antisense ASIC1a-RNA, intrathecal administered in mice were shown to affect both phases of the test.
methodsThe mouse formalin test was performed on C57/BL6 7- to 9-week-old mice. Behavioral tests were conducted and tissue was extracted to detect proteins (ASIC1 and pERK) and ASIC1-mRNA and mir485-5p levels.
resultsThe injection of formalin was accompanied by an increase in ASIC1 levels. This was detected at the contralateral anterior cingulate cortex (ACC) compared to the ipsilateral side, and both sides of the ACC of vehicle-injected animals. At the spinal cord and dorsal root ganglia, ASIC1 levels followed a gradient stronger at lumbar (L) 3 and decreased towards L5. Gender differences were detected at the ACC; with female mice showing higher ASIC1a levels at the ACC. No significant changes in ASIC1-mRNA levels were detected. Evidence suggests ASIC1 upregulation depends on regulatory microRNAs.
conclusionThis work highlights the important role of ASIC1 in pain and the potential role of pharmacological therapies aimed at this channel.
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