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FGF13 Selectively Regulates Heat Nociception by Interacting with Nav1.7.

Neuron (2017-02-07)
Liu Yang, Fei Dong, Qing Yang, Pai-Feng Yang, Ruiqi Wu, Qing-Feng Wu, Dan Wu, Chang-Lin Li, Yan-Qing Zhong, Ying-Jin Lu, Xiaoyang Cheng, Fu-Qiang Xu, Limin Chen, Lan Bao, Xu Zhang
RESUMEN

The current knowledge about heat nociception is mainly confined to the thermosensors, including the transient receptor potential cation channel V1 expressed in the nociceptive neurons of dorsal root ganglion (DRG). However, the loss of thermosensors only partially impairs heat nociception, suggesting the existence of undiscovered mechanisms. We found that the loss of an intracellular fibroblast growth factor (FGF), FGF13, in the mouse DRG neurons selectively abolished heat nociception. The noxious heat stimuli could not evoke the sustained action potential firing in FGF13-deficient DRG neurons. Furthermore, FGF13 interacted with the sodium channel Nav1.7 in a heat-facilitated manner. FGF13 increased Nav1.7 sodium currents and maintained the membrane localization of Nav1.7 during noxious heat stimulation, enabling the sustained firing of action potentials. Disrupting the FGF13/Nav1.7 interaction reduced the heat-evoked action potential firing and nociceptive behavior. Thus, beyond the thermosensors, the FGF13/Nav1.7 complex is essential for sustaining the transmission of noxious heat signals.

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Sigma-Aldrich
Anti-c-Myc antibody produced in rabbit, ~0.5 mg/mL, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
Anti-Sodium channel Nav1.7 Antibody, clone N68/6, clone N68/6, from mouse