"Transplant-mediated repair of spinal cord GABAergic inhibitory circuitry to treat the "disease" of neuropathic pain"

Dr. Basbaum is interested in the mechanisms through which tissue or nerve injury result in persistent/chronic pain. A major question is the extent to which different features of the pain experience are evoked by the activity of selected subsets of "pain fibers" (i.e. nociceptors) vs. by differential patterns of activity generated across multiple populations of afferents. To understand the functional significance of the molecular complexity of the nociceptor, he studies pain behavior in mice with deletions of different genes that code for tranducers of injury stimuli or that code for different neurotransmitter receptors and second messenger molecules. Among the many molecules that he has studied are the TRP channels (including TRPV1 and TRPM8) as well as major second messenger molecules, notably the gamma isoform of protein kinase C, which is implicated in the development of nerve injury-induced neuropathic pain.