Chronic pain is often associated with injuries to peripheral nerves. These injuries may be traumatic, such as those following back injury, automobile accident, or gun shot wound. Alternately, they may result from pressure applied by bony protuberances, vascular malformations or scar tissue that have formed for unknown reasons. Regardless of the nature of predisposing events, individuals often report spontaneous burning pain and hyperesthesia. Animal models have indicated that peripheral nerve injuries produces changes in cellular activity and reactivity in dorsal root ganglia (DRG). The cause of such changes are not known. Our laboratory has been studying the properties of a novel protein that is expressed, in humans, at sites of chronic pain. In our proposal, we will use whole cell patch clamp techniques to assess changes in K+ currents and excitability of DRG cells following exposure to a C terminal peptide effector of this novel protein.
