Recently, autosomal dominant mutations in SCN11A, which encodes Nav1.9, a voltage-gated sodium channel subunit alpha type 9, have been found in pain syndromes, including episodic familial pain syndrome [11-13].
The structure of Nav1.9 was predicted and visualized as described by Omasits U.
Wood, "The role of Nav1.9
channel in the development of neuropathic orofacial pain associated with trigeminal neuralgia," Molecular Pain, vol.
Su et al., "Electroacupuncture reduces carrageenan- and CFA-induced inflammatory pain accompanied by changing the expression of Nav1.7 and Nav1.8, rather than Nav1.9
, in mice dorsal root ganglia," Evidence-Based Complementary and Alternative Medicine, vol.
By use of a patch clamp, we evaluated the effects of menthol application on tetrodotoxin (TTX)-resistant Nav1.8 and Nav1.9
channel subtypes in DRG neurons, and on TTX-sensitive Na() channels in immortalized DRG neuron-derived F11 cells.
The specific isoforms Nav1.8 and Nav1.9
play a key role in the generation and maintenance of inflammatory pain.
A large variety of Nav subtypes from DRG cells, including tetrodotoxin- (TTX-) sensitive channels Nav1.1, Nav1.2, Nav1.6, and Nav1.7 and TTX-resistant channels Nav1.8 and Nav1.9
, have been evaluated for involvement in epilepsy [35, 36].
Loescher et al., "Correlation of Nav1.8 and Nav1.9
sodium channel expression with neuropathic pain in human subjects with lingual nerve neuromas," Molecular Pain, vol.
For example, Nav1.6 is the variety present at the nodes of Ranvier, Nav1.5 is in the heart muscle, and others such as Navl.7, Nav1.8 and Nav1.9
are predominant in pain-sensing neurons.
Developmental expression of the TTX-resistant voltage-gated sodium channels Nay1.8 (SNS) and Nav1.9
(SNS2) in primary sensory neurons.
In addition to its cancer program, the company has a chronic pain program that targets a sodium ion channel called Nav1.9
, selectively expressed in the peripheral nervous system.
Other studies of postmortem tissue from injured human nerves and chronic neurogenic pain report significant changes in the level and tissue distribution of Nav1.8 and Nav1.9
sodium channels after nerve injury (Coward et al., 2000).