My research focuses on the molecular and physiological processes that initiate and maintain chronic pain. In particular, we are examining alterations in the function of the N-Methyl-D-Aspartate (NMDA) class of excitatory amino acid receptor in the spinal cord and the vanilloid receptor – the protein responsible for detecting the burning sensation produced by hot chili peppers – in the periphery following persistent stimulation. The NMDA receptor performs the function of an amplifier in the spinal cord to enhance pain signals, whereas the vanilloid receptor detects pain from heat, inflammation, and chemicals throughout the body. These studies examine changes in the phosphorylation status of these two receptors and alterations in subunits and splice variants as a result of painful experiences. These studies also examine the interaction of the NMDA receptor and vanilloid receptor with endogenous neuropeptides that are released during chronic pain. The ultimate goal of our work is to develop novel strategies to avoid the induction of chronic pain and new therapies to treat chronic pain once it is established.