Mild traumatic brain injuries (mTBI) are common mechanical traumas to the head that result in either no or transient (<30 min) loss of consciousness, representing approximately 80% of TBIs reported worldwide1,2. Increasing incidence of mTBI make them a growing public health concern1. Despite being termed ‘mild’, approximately 30% of mTBI patients experience long-term functional deficits1,3. Importantly, the effects of pediatric mTBI (pmTBI) are understudied compared to the adult population1,2. In addition, mTBI symptoms and pathophysiology is sexually dimorphic at both clinical and preclinical levels. To better understand the mechanisms and longitudinal effects of pmTBI, and associated sex differences, this thesis utilized both male and female C57B6 mice in a translational preclinical model of pmTBI4,5. Using the closed head injury with long term disorders (CHILD) model of pmTBI we performed whole-cell patch-clamp electrophysiology experiments to investigate intrinsic neuronal excitability changes at acute and chronic timepoints post-injury. Our results indicate increased excitability of hippocampal neurons at post injury day 0 (PI0) in females that appears to resolve by post-injury day 30-35 (PI30) with no recurrent changes at PI1YR. pmTBI also increased ionic dysregulation in an excitotoxicity assay specifically in males at PI30. The increased excitability in females suggests altered hippocampal network connectivity immediately following injury, but due to the sensitive time in pediatric development could have lifelong functional consequences. Further, pmTBI-mediated increases in ionic dysregulation in males suggests that injury could prime neurons to be more vulnerable to secondary injuries or insults later in life.