Post-traumatic epilepsy (PTE) is a common, serious, long-term complication of traumatic brain injury (TBI). However, only a minority of individuals will develop epilepsy after a TBI, and the contribution of genetic predisposition to the risk of acquired epilepsy warrants further exploration. In this study, we examined whether innate, genetically determined differences in seizure susceptibility between seizure-prone FAST and seizure-resistant SLOW rat strains would influence chronic behavioral and PTE outcomes after experimental TBI. We hypothesized that FAST rats would show increased vulnerability to PTE and poorer neurobehavioral outcomes. Using the lateral fluid percussion injury model, we first determined the optimal injury parameters to generate a mild-moderate TBI in young adult FAST rats, which had previously shown high mortality to severe TBI. Then, FAST and SLOW rats underwent TBI or sham surgery, and a series of behavioral tests were performed either acutely (within 4 weeks) or chronically (more than 22 weeks) post-injury. Acutely, FAST rats showed an increased physiological response to TBI with a longer apnea duration, delayed pain response, and delayed self-righting, as well as increased acute seizure-like behavior compared to SLOW rats. Conversely, SLOW rats showed greater neuromotor deficits and weight loss sub-acutely compared to FAST rats. Chronically, while strain-specific phenotypes were observed (e.g., FAST rats showing increased anxiety-like behavior, altered nociceptive responses, and polydipsia), no TBI effects were detected. Analysis of continuous video-electroencephalographic recordings over a 1-month period starting at 6 months post-TBI did not reveal any spontaneous seizures. However, periodic epileptiform discharges were only found in FAST rats that had a TBI. Together, these findings reflect fundamental differences in chronic behavior and epileptiform discharges as a result of innate distinctions in epileptogenic susceptibility in FAST versus SLOW rats. However, a lack of spontaneous seizure activity or chronic neurobehavioral deficits in TBI animals confounded our ability to address the initial hypothesis, such that alternative injury models may be more suitable to study genetic contributions to the development of PTE.