Date of Graduation


Document Type


Degree Type



Eberly College of Arts and Sciences



Committee Chair

Cole Vonder Haar

Committee Member

Steven Kinsey

Committee Member

Rudolph Castellani


Traumatic brain injury (TBI) can cause chronic psychiatric-like impairments that may be driven by inflammation in the brain. In the current study, inflammation was upregulated using a high-fat diet (HFD) to assess the role of inflammation in TBI-induced deficits. Rats were randomly assigned to receive an HFD or calorie-matched low-fat diet (LFD) for the duration of the experiment. After two weeks of free access to their respective diets, rats began behavioral training on the Rodent Gambling Task (RGT), during which they were allowed to freely choose to nosepoke in one of four holes in a standard operant chamber. Responses in each hole were associated with different probabilities and magnitudes of reinforcement (sucrose pellets) or punishment (timeout from reinforcement); thus, choices could be classified as either risky or optimal. Premature responses (i.e., nosepokes made before the trial began) were used as a measure of motor impulsivity. After behavior on the RGT stabilized, rats received either a frontal TBI or a sham procedure and continued post-injury testing for 10 weeks. TBI rats substantially decreased in optimal choice but increased in risky choices and motor impulsivity. However, deficits induced or exacerbated by the HFD were inconsistent and low in magnitude. After the behavioral portion of the study, rats were transcardially perfused. The HFD and TBI in combination interacted to increase neuroinflammation, as measured by microglia count. Increases in microglia unaccompanied by changes in behavior indicated that inflammation may simply be a symptom of brain injury and not a driver of psychiatric-like deficits. Thus, further evidence is required to characterize the role of inflammation in cognitive impairment both within and outside the context of brain injury.