Transmission in pain pathways can be profoundly and protractedly modified by experience. Both presynaptic and postsynaptic changes in transmission are thought to contribute to the development of chronic pain conditions. Studies in our lab are aimed at determining the cellular and molecular mechanisms responsible for these effects. We utilize a variety of approaches, including behavioral analysis, patch clamp electrophysiology, optogenetics, molecular and biochemical analysis, and genetics to address these questions in mouse models of chronic pain conditions.

Current studies focus on studies of maladaptive plasticity in three main regions of the pain neuraxis (primary sensory neurons, dorsal horn neurons, and the amygdala). Current active areas of study

 include:
          • Modulation of nociception by metabotropic glutamate receptors (mGluRs) expressed in primary afferent neurons.
          • ERK signaling and modulation neuronal excitability in spinal cord dorsal horn neurons.
          • The role of mGluRs and their signaling pathways in amygdala plasticity associated with chronic pain.
          • Epigenetic mechanisms of chronic pain and analgesia
          • Development of novel micro-scale devices and their implementation in optogenetic studies of chronic pain

The goal of these studies is to understand how synaptic transmission in the spinal cord and other pain processing centers is modulated in the context of chronic pain. We hope to use this knowledge to develop new treatments for the prevention and management of persistent pain associated with injury and disease.