Sodium channels Na1.7, Na1.8 and pain; two distinct mechanisms for Na1.7 null analgesia.

Genetic deletion and pharmacological inhibition are distinct approaches to unravelling pain mechanisms, identifying targets and developing new analgesics. Both approaches have been applied to the voltage-gated sodium channels Na1.7 and Na1.

Mapping protein interactions of sodium channel Na1.7 using epitope-tagged gene-targeted mice.

The voltage-gated sodium channel Na1.7 plays a critical role in pain pathways. We generated an epitope-tagged Na1.

Voltage-gated sodium channels and pain-related disorders.

Voltage-gated sodium channels (VGSCs) are heteromeric transmembrane protein complexes. Nine homologous members, SCN1A-11A, make up the VGSC gene family. Sodium channel isoforms display a wide range of kinetic properties endowing different neuronal types with distinctly varied firing properties.

Endogenous opioids contribute to insensitivity to pain in humans and mice lacking sodium channel Nav1.7.

Loss-of-function mutations in the SCN9A gene encoding voltage-gated sodium channel Nav1.7 cause congenital insensitivity to pain in humans and mice. Surprisingly, many potent selective antagonists of Nav1.

The utility of zebrafish to study the mechanisms by which ethanol affects social behavior and anxiety during early brain development.

Exposure to moderate levels of ethanol during brain development has a number of effects on social behavior but the molecular mechanisms that mediate this are not well understood. Gaining a better understanding of these factors may help to develop therapeutic interventions in the future. Zebrafish offer a potentially useful model in this regard.