The role and mechanism of fibroblast growth factor FGF13 in itching were found

The Journal of Neuroscience published a research paper entitled FGF13 Is Required for Histamine-Induced Itch Sensation by Interaction with NaV1.7.
The study was carried out by Zhang Xu, Research Group of the Center for Excellence in Brain Science and Intelligent Technology of the Chinese Academy of Sciences (Institute of Neuroscience), National Key Laboratory Researcher of Neuroscience, and Bao Wei Research Group, Research Group of the National Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science of the Chinese Academy of Sciences (Institute of Biochemistry and Cell Biology).
early work by the
team found that the mice lost their response to injury-based heat stimulation (Yang et al.) after the selectively high expression of a non-secretive fibroblast cell growth factor (Fibroblast growth factor, FGF) 13 in the injury sensory neurons of the research team found that the mice had lost their response to the damaged heat stimulation (Yang et al.) Neuron, 2017).
previous studies have also shown that activating the injury-like sensory neurons in DRG can produce itchy sensations.
, however, it is not clear whether FGF13 functions in itch perception.
team used FGF13-specific knock-out mice in DRG's injury-causing sensory neurons to find that the number of scratches caused by histamines decreased significantly in the mice, with little scratching in the mice recorded in the first 20 minutes.
using cell electrophysiology and calcium imaging detection techniques, it was found that the percentage of DRG neurons responding to histamine after FGF13 was missing decreased significantly.
the in-cell signaling pathline needs to be combined with the corresponding subjects, and there are four known histamines, including H1R, H2R, H3R and H4R.
By detecting the actional position reaction of four different histamine-induced mediators stimulated by histamines, combined with different histamine-like agents causing different scratching behavior in mice with FGF13 deficiency, it was found that H1R was the main subject of the downstream signaling pathline in which FGF13 participated after the mediated histamine stimulation.
further studies have shown that FGF13 has no direct physical or functional effect on H1R.
previous studies by the team have shown that FGF13 can affect the generation of neuron motor potions by combining voltage-gateed sodium ion channel NaV1.7 (Yang et al., Neuron, 2017).
to explore the role of NaV1.7 in the itchy response mediated by FGF13, the team further used cellular electrophysiological records to find sodium channel antagonist pufferfish toxin TTX and NaV1.7 specific antagonist antagonist The agents can significantly reduce the neuron's reaction to histamine, block the interaction between FGF13 and NaV1.7, not only reduce the neuron's reaction to histamine, but also produce behavioral ideologies similar to the decrease in the number of scratches in mice with FGF13.
In addition, the study found that FGF13-missing mice also experienced varying degrees of decline in scratch response to itching agents such as nonhistamines (5-HT and chloroquine CQ) and in the clinical chronic itching simulated by DNFB.
the study sheds light on the new function of FGF13 in the peripheral nervous system to mediat itchy feelings by interacting with Nav1.7.
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