Posted on May 26, 2014
Researchers from Duke University Medical School, writing in the journal Cell report their findings from an investigation of voltage-sensitive sodium channels in cell membranes. These channels open or close depending on the electric signal emitted by the cell. One of these, called the Nav1.7 subtype, is responsible for sensing pain. The team then developed an antibody that can bind to the Nav1.7 sodium channel and stabilize its closed state, leading to lessened pain sensitivity.
Repeating the study with mice bred to experience neuropathic and inflammatory pain, the researchers were able to replicate the cultured cell results; in addition to diminished pain, the mice that had been given the antibody showed no dependence on it once it was removed. The findings may open the way to development of new pharmacologic approaches that avoid the adverse effects of opioid medications. Read a news story, with link to the study abstract, here.