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Related Experiment Video

Updated: Jun 24, 2026

Tissue Preparation and Immunostaining of Mouse Sensory Nerve Fibers Innervating Skin and Limb Bones

Tissue Preparation and Immunostaining of Mouse Sensory Nerve Fibers Innervating Skin and Limb Bones

Published on: January 26, 2012

Two novel SCN9A mutations causing insensitivity to pain.

K B Nilsen¹, A K Nicholas, C G Woods

¹Department of Neuroscience, Norwegian University of Science and Technology, Edvard Griegs gate 8, 7489 Trondheim, Norway. kristian.b.nilsen@ntnu.no

|March 24, 2009

Summary

This summary is machine-generated.

Congenital insensitivity to pain is a rare genetic disorder. This study identifies two new SCN9A gene mutations causing loss of function in the Nav1.7 channel, leading to pain insensitivity and anosmia.

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Area of Science:

Genetics
Neuroscience
Physiology

Background:

Pain sensation is crucial for survival.
Channelopathies can lead to congenital insensitivity to pain.
Mutations in the SCN9A gene affecting the Nav1.7 channel are implicated.

Observation:

A patient presented with congenital insensitivity to pain.
This patient exhibited anosmia (loss of smell).

Findings:

Two novel mutations in the SCN9A gene were identified in the patient.
These mutations cause a loss of function in the Nav1.7 voltage-gated sodium channel.
The identified mutations are linked to channelopathy-associated insensitivity to pain.

Implications:

Understanding Nav1.7 channel function is key to pain perception.
Novel SCN9A mutations expand the known genetic basis of pain insensitivity.
The frequent co-occurrence of anosmia warrants further investigation in SCN9A channelopathies.