The Gain-of-Function R222S Variant in Scn11a Contributes to Visceral Hyperalgesia and Intestinal Dysmotility in Scn11a ^R222S/R222S Mice.

ABSTRACT:

Background

The SCN11A gene encodes the α-subunit of the Nav1. 9 channel, which is a regulator of primary sensory neuron excitability. Nav1.9 channels play a key role in somatalgia. Humans with the gain-of-function mutation R222S in SCN11A exhibit familial episodic pain. As already known, R222S knock-in mice carrying a mutation orthologous to the human R222S variant demonstrate somatic hyperalgesia. This study investigated whether Scn11a ^R222S/R222S mice developed visceral hyperalgesia and intestinal dysmotility.

Methods

We generated Scn11a ^R222S/R222S mice using the CRISPR/Cas9 system. The somatic pain threshold in Scn11a ^R222S/R222S mice was assessed by Hargreaves' test and formalin tes

SUBMITTER: Zhao C 

PROVIDER: S-EPMC9197071 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature