Papers of the Week

The malfunction and misregulation of voltage-gated sodium channels (Na s) underlie in large part the electrical hyperexcitability characteristic of chronic inflammatory and neuropathic pain. Na s are responsible for the initiation and propagation of electrical impulses (action potentials) in cells. Tissue and nerve injury alter the expression and localization of multiple Na isoforms, including Na 1.1, 1.3, and 1.6-1.9, resulting in aberrant action potential firing patterns. To better understand the role of Na regulation, localization, and trafficking in electrogenesis and pain pathogenesis, a number of chemical and biological reagents for interrogating Na function have been advanced. The development and application of such tools for understanding Na physiology are the focus of this review.