Postdoctoral in Cell Biology & Neuroanatomy at University of Minnesota, Minneapolis, MN. PhD in Anatomy & Neurobiology at University of Vermont, Burlington, Vermont. B.S in Biology, Kansas State University, Manhattan, KS.

To evaluate glutamate metabolism in spinal systems during various injury, inflammatory, and pain conditions. Glutamate is the major excitatory neurotransmitter in the nervous system, but the production and degradation of glutamate is poorly understood in the peripheral nervous system. My research has been carried out in three areas: 1. Primary sensory neurons under normal and painful, inflammatory and neuropathic conditions. 2. Spinal processing of inflammatory nociceptive information from the viscera and somatic structures. 3. Response of neurons to spinal injury and CNS inflammation. Pain is a debilitating complication of chronic inflammation and nerve injury. These chronic pains are difficult to treat for long periods of time. Our current research efforts have been directed toward glutamate metabolism during chronic inflammatory pain. We have demonstrated that the glutamate-glutamine cycle, a CNS enzyme system for the production and degradation of glutamate, is present in the peripheral nervous system. We have shown that chronic inflammation causes long-term increases in glutaminase, the enzyme for glutamate synthesis, and glutamate levels in primary sensory neurons and their peripheral nerve fibers. Increased glutamate production in peripheral nerve fibers is responsible, in part, for painful responses observed in chronic inflammations, such as rheumatoid arthritis. We have determined that peripheral inhibition of glutaminase provides long-lasting pain relief in animals with chronic inflammation.