Abstract: A common neurophysiological mechanismn underlying both posttraumatic epilepsy and neuropathic pain is the hyperexcitability of the affected neural network. Although cnventional treatment strategies for these disabling disorders primarily focus on inihibiting such hyperexcitability, the fundamental question of what drives the injured nervous system to become hyperexcitable remains unanswered. Since neurotrauma can damage the brain (which may induce epileptogenesis) or the somatosensory pathways from peripheral nerve to the brain (which often causes neuropathic pain), the resulting loss of neurons or afferent input can cause network hyperexcitability through a maladaptive homeostatic plasticity regulation. This well-established mechanism works intrinsically to counterbalance the loss of brain activity or function. In other words, the loss of activity after neurotrauma drives the development of hyperexcitability. In this talk, we will present findings on the role of homeostatic plasticity in both disorders. Following an overview of current hypertheses and treatement strategies, we will discuss how homeostatic plasticity mechanism of the cerebral cortex contributes to the development of cortical hyperexcitability, and how targeting activity enhancement (rather than activity inhibition) may offer a novel strategy for the prevention or treatment of posttraumatic epilepsy and neuropathic pain.

Bio:  Dr. Jin is an Associate Professor of the Department of Anatomy, Cell Biology and Anatomy, a member of the Stark Neurosciences Research Institute, and a member of the Neurotrauma Research Group at Indiana University School of Medicine. His research interest focuses on understanding cortical plasticity and neuroinflammation in the mechanisms of posttraumatic epilepsy and neuropathic pain and developing novel treatments and prevention for these diseases.

The seminar series is sponsored by Purdue's Center for Paralyis Research and Plexon.

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