Sensory neuron-derived NaV1.7 contributes to dorsal horn neuron excitability.

Science Advances
S. R. A. AllesJohn N Wood

Abstract

Expression of the voltage-gated sodium channel NaV1.7 in sensory neurons is required for pain sensation. We examined the role of NaV1.7 in the dorsal horn of the spinal cord using an epitope-tagged NaV1.7 knock-in mouse. Immuno-electron microscopy showed the presence of NaV1.7 in dendrites of superficial dorsal horn neurons, despite the absence of mRNA. Rhizotomy of L5 afferent nerves lowered the levels of NaV1.7 in the dorsal horn. Peripheral nervous system-specific NaV1.7 null mutant mice showed central deficits, with lamina II dorsal horn tonic firing neurons more than halved and single spiking neurons more than doubled. NaV1.7 blocker PF05089771 diminished excitability in dorsal horn neurons but had no effect on NaV1.7 null mutant mice. These data demonstrate an unsuspected functional role of primary afferent neuron-generated NaV1.7 in dorsal horn neurons and an expression pattern that would not be predicted by transcriptomic analysis.

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Citations

Feb 27, 2021·The Journal of Pain : Official Journal of the American Pain Society·Pedro AlvarezJon D Levine
Mar 31, 2021·Nature Reviews. Neuroscience·George Goodwin, Stephen B McMahon
Mar 30, 2021·Neuroscience Letters·Yaping XueClaire Gaveriaux-Ruff
May 14, 2021·Pain Reports·Michael J LacagninaPeter M Grace
Nov 11, 2021·Science Translational Medicine·Song CaiRajesh Khanna

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Methods Mentioned

BETA
immunoprecipitation
Tandem Affinity Purification
confocal microscopy
electron microscopy

Software Mentioned

Zeiss Zen Blue microscopy
Origin Lab
Clampex
Bayesian Quantal Analysis suite
GraphPad Prism
Excel

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