Cognitive deficits are a common consequence of both traumatic brain injury (TBI) and temporal lobe epilepsy (TLE) and are often treatment refractory. Learning and memory impairments are especially common in TBI and TLE and are thought to be driven in part by pathological changes to hippocampal circuits that support these processes. Interestingly, both disorders have some overlapping hippocampal circuit pathologies including regional-specific cell loss, increased neurogenesis, mossy fiber sprouting, interneuron loss and dysfunction, and disruptions to hippocampal afferent inputs all of which may disrupt physiological processes that support learning and memory. Additionally, seizures can be a shared consequence of TBI and TLE and may further exacerbate cognitive deficits. Disentangling how hippocampal circuit pathologies and seizures independently contribute to learning and memory deficits is difficult because circuit pathologies can give rise to seizures, and seizures can induce pathological changes in hippocampal circuits. This body of work attempts to separate these two phenomena and explore i) how behaviorally relevant physiological process in the hippocampus are disrupted in TBI and ii) whether seizures generated by experimentally increasing dentate granule cell (DGC) excitability impair spatial memory. Using laminar electrodes, we found a loss of hippocampal theta and gamma oscillatory power and coupling in a model of TBI likely driven by decreased entrainment of interneurons to these oscillations. We believe these changes contribute to learning and memory deficits following TBI. Additionally, we found that increasing DGC excitability with chemogenetics induced seizures and memory deficits in uninjured, non-epileptic mice, providing support for a specific role of seizures in TLE-associated cognitive deficits in the absence of hippocampal pathologies. Results from these studies show that pathological changes to hippocampal circuits in TBI disrupt physiological processes known to support learning and memory, and that seizures in the absence of pathological circuit disruptions can impair memory. Results from these studies may provide insight into future circuit-based neuromodulation therapies that specifically target TBI or TLE associated cognitive deficits arising from pathological changes to hippocampal circuits or from seizures.