Pain & CNS behavior CRO  
Research News
February 2017
Nav1.7 has been yet described to be involved in heat nociception, in mouse as well in human. Using conditional knock-out mice for fgf13, Yang and coll have nicely demonstrated a pivotal role of Fgf13 interacting with the voltage-gated sodium Nav1.7 in somato-sensory neurons to permit the maintainance of action potential firing under noxious heat stimulation (Yang et al. 2017, Neuron). Dorsal root ganglion specific conditional knock-out mice for fgf13 (SNS-CRE:Fgf13 -/y) are completely insensitive to heat stimulation using different behavioral tests (tail flick test, hot plate test, hargreaves in acute as well in CFA inflammatory model, two-temperature choice test). Interestingling, mechanical or chemical pain are not affected in this mice model. Absence of response to heat stimulation is due to a heat-evoked action potential decrease when noxious temperature are reached. Using a TAT-driving rescue strategy with FGF13B (the cytoplasmic form of Fgf13), they have shown that intrathecal injection of this chimeric protein is able to restore a noxious-heat response. Biochemical experiments have demonstrated an interaction between Fgf13 and a 20 aa region in the C-terminus part of Nav1.7. This interaction maintains plasma membrane localisation of Nav1.7 channel under noxious heat stimulation, necessary for correct heat-evoked action potential firing. 
This key role of Fgf13 and Nav1.7 open new opportunities for treatment of patients affected by abnormal heat-sensing pathologies or for the well-being of burn victims