Allison Moore

Background

About Allison Moore

I am a fourth year Ph.D. candidate at Indiana University School of Medicine. My research interest is in the role of homeostatic plasticity in epileptogenesis following traumatic brain injury (TBI). Our lab hypothesizes that cell death and functional neuronal inactivity after TBI causes a compensatory response that triggers homeostatic regulatory mechanisms which become pathological, leading to hyperexcitability and synchronous bursting, and eventually posttraumatic epilepsy (PTE). If this hypothesis is correct, then targeting homeostatic plasticity by enhancing activity, rather than inhibiting activity as most anti-epileptic drugs (AEDs) do, could alleviate PTE. We use a rodent partial cortical defferentation ("undercut") model of PTE, in which a penetrative TBI is induced via a transcortical cut in the white matter, creating a neocortical "island" where afferent input is severed and eventually becomes epileptic. I use graph theory and complex network analysis to characterize dynamic changes in the functional cortical excitatory network after TBI from in vivo 2-photon imaging in Thy1-GCaMP mice, where we visualize calcium as a proxy for action potential activity in cortical neurons. These tools can be applied to monitor changes in functional activity and network connectivity, which can give us a sense of how reorganization may be occurring during epileptogenesis. Our lab additionally uses optogenetic tools to enhance cortical activity in ChR2 mice to target homeostatic plasticity after TBI and alleviate PTE. Seizure susceptibility paradigms like the pentylenetetrazole (PTZ) test, as well as continuous EEG recording to probe for spontaneous seizure events are used to measure epilepsy severity.