ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020
FGF13 Is Required for Histamine-Induced Itch Sensation by Interaction with Na
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Mechanisms of pruritus and advances in traditional Chinese medicine therapy (Review).Molecular medicine reports · 2026Review
- The Role of Fibroblasts in Atopic Dermatitis: Establishing Proinflammatory Microenvironments and Mediating Cellular Crosstalk.Journal of inflammation research · 2025Review
- The role of nociceptive neurons in allergic rhinitis.Frontiers in immunology · 2024Review
- Somatosensory neurons express specific sets of lincRNAs, and lincRNA CLAP promotes itch sensation in mice.EMBO reports · 2023Article
- Fibroblast growth factor homologous factor 2 attenuates excitability of DRG neurons.Journal of neurophysiology · 2022Article
- Shared nociceptive dorsal root ganglion neurons participating in acupoint sensitization.Frontiers in molecular neuroscience · 2022Article
- Context dependent roles of FGF13B-NaNeurobiology of pain (Cambridge, Mass.)Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Itch can be induced by activation of small-diameter DRG neurons, which express abundant intracellular fibroblast growth factor 13 (FGF13). Although FGF13 is revealed to be essential for heat nociception, its role in mediating itch remains to be investigated. Here, we reported that loss of FGF13 in mouse DRG neurons impaired the histamine-induced scratching behavior. Calcium imaging showed that the percentage of histamine-responsive DRG neurons was largely decreased in FGF13-deficient mice; and consistently, electrophysiological recording exhibited that histamine failed to evoke action potential firing in most DRG neurons from these mice. Given that the reduced histamine-evoked neuronal response was caused by knockdown of FGF13 but not by FGF13A deficiency, FGF13B was supposed to mediate this process. Furthermore, overexpression of histamine Type 1 receptor H1R, but not H2R, H3R, nor H4R, increased the percentage of histamine-responsive DRG neurons, and the scratching behavior in FGF13-deficient mice was highly reduced by selective activation of H1R, suggesting that H1R is mainly required for FGF13-mediated neuronal response and scratching behavior induced by histamine. However, overexpression of H1R failed to rescue the histamine-evoked neuronal response in FGF13-deficient mice. Histamine enhanced the FGF13 interaction with Na
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