Defense Date


Document Type


Degree Name

Doctor of Philosophy


Anatomy & Neurobiology

First Advisor

John T. Povlishock, PhD

Second Advisor

William C. Broaddus, MD PhD

Third Advisor

Raymond Colello, PhD

Fourth Advisor

Kimberle Jacobs, PhD

Fifth Advisor

Dong Sun, PhD


Traumatic brain injury (TBI) is a leading cause of morbidity and mortality nationwide. Prevalence of mild TBI (mTBI) vastly outnumbers more severe forms however the associated morbidity has only recently gained public attention. Visual dysfunction is a significant component of mTBI associated morbidity with recovery of function linked with improvement in global outcomes. Examination of sensory and motor pathways in other brain injury paradigms support that recovery is largely dependent on adaptive plasticity of remaining connections. Current examinations of visual function recovery following mTBI is limited to identifying evidence for recovery and objective evidence for adaptive plasticity is limited. Therefore, to understand the mechanisms behind visual recovery in mTBI, we utilize a mouse model to examine the changes in the downstream target of retinal ganglion cells (RGC) in the formed vision pathway, the lateral geniculate nucleus (LGN). Using techniques designed to identify structural changes as well as electrophysiologic connectivity we aimed to identify if deafferentation due to experimental mTBI is met with adaptive structural and electrophysiologic reorganization of inputs to LGN relay cells, to determine if they may contribute to recovery of vision over time. Examination of ensuing deafferentation in LGN was performed using a combination of anterograde tract tracing with cholera toxin B conjugated fluorescent probes, immunohistochemistry targeting retinal ganglion cell axon terminals, and a transgenic mouse in which a subpopulation of retinal ganglion cells are labelled with green fluorescent protein. Our studies were designed to capture structural reorganization in specific subpopulations of retinal ganglion cells and determine if ensuing reorganization violated projection patterns established during normal development and refinement of the retinal geniculate pathway. Additionally, our studies examined the electrophysiologic responses of relay neurons in the lateral geniculate nucleus to stimulation of the optic tract as a function of time following injury. Using ex-vivo patch clamp recording of LGN relay neurons, we examined responses of these cells to stimulation of the optic tract following mTBI. Our findings demonstrated intact short-term depression at the retinal geniculate synapse following injury, which is a mechanism through which LGN relay neurons establish functional connectivity from retinal inputs. This innate mechanism of short-term plasticity likely uncovers latent connectivity between the remaining retinal inputs and LGN relay neurons to provide new connectivity for functional recovery. These studies support the premise that recovery of function in the visual axis following mild TBI is dependent on adaptive structural and electrophysiologic reorganization within the lateral geniculate nucleus.


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