The major focus of research in my laboratory involves examining the cellular mechanisms that mediate the peripheral sensitization that occurs secondary to inflammation. This sensitization of small diameter sensory neurons results in enhanced release of neurotransmitters and is believed to be a major component of neurogenic inflammation, enhanced pain perception in inflammation, and neuropathy.
Studies center on elucidating the signal transduction cascades that mediate an increase in transmitter release produced by inflammatory mediators and on determining the targets for post translational modification after activation of various transduction cascades.
Additional studies examine the mechanism by which cancer therapies alter the sensitivity of sensory neurons, a phenomenon that contributes to sensory neuropathy.
Recently, work in my laboratory has focused in part on the development of viral constructs and implementation of procedures to use genetic manipulation of neurons to alter expression of various components of intracellular signaling cascades. Signal transduction regulating sensitization of sensory neurons. Our current research involves determining the cellular mechanisms mediating peripheral sensitization that occurs during tissue trauma and inflammation and the enhanced release of neurotransmitters from pain-sensing (nociceptive) sensory neurons that accompanies this sensitization
