The focus of my recent research includes the study of the neural mechanism of acute and chronic pain. The general strategy used in our lab is to identify behavior phenotype by observation, and to correlate morphological and functional changes in the nervous system.
For the study of chronic pain, our lab is presently concentrating on neuropathic pain models of the rodents. Two types of models are used, one for sciatica and one for trigeminal pain. The three cardinal symptoms of the neuropathic pain patients are spontaneous pain, abnormal pain response to light stimuli (allodynia), and enhanced pain response to light pain (hyperalgesia). We use rodent neuropathic pain models to observe these three types of behaviors first. Next we used MRI and PET imaging techniques to search for forebrain areas that show activity changes correlate with neuropathic pain behaviors. This is complemented by chronic electrophysiological recording experiments to track the brain activity changes longitudinally. In addition, treatments, such as drugs and electrical stimulations, are used to alleviate the symptoms and at the same time, correlate with brain activity changes.
Starting from 2016, we begin a new project probing the peripheral changes of primary afferent fibers after nerve injuries, such as compression and intoxication by chemotherapy and diabetes mellitus. Structure changes of the free nerve endings and first synapse in the spinal cord are quantified with advanced two-photon and harmonic generation microscopic methodologies. These dynamic changes are correlated with pain behavioral changes. Our goals are to identify key neural changes related to pain function. These changes may be used as biomarkers for diagnosis and treatment.