INTRODUCTION: Traumatic brain injury (TBI) affects millions of people, representing a major public health concern. Several important cognitive functions altered by TBI depend on the hippocampus, where new neurons are born throughout life. Functional plasticity of synaptic networks in the hippocampus has been implicated in the development of posttraumatic epilepsy after TBI. The hippocampus dentate gyrus (DG) acts as a “gatekeeper” and “filter” of aberrant or excessive input information. DG function is directly determined by a delicate balance between neuronal excitation and inhibition and TBI can cause changes in this state of equilibrium. It has been postulated that TBI‑induced hyperexcitation of preexisting DG granule cells (GCs) can affect adult hippocampal neurogenesis (AHN) and induce long-term changes in both neural stem cells (NSCs) and newborn neurons, and those alterations can contribute to hippocampal dysfunction. AIM(S): We aim to understand what particular changes TBI induces at the cellular, molecular, and electrophysiological levels in preexisting GCs, NSCs, and newborn neurons, using a model of controlled cortical impact. RESULTS: Observed changes in spontaneous excitatory currents (sEPSCs) frequency indicate remodeling of excitatory input, likely expressed as an increase in the number of excitatory synapses. Those changes are accompanied by a decrease in spontaneous inhibitory currents (sIPSCs) frequency, indicating a loss of GABAergic neurons. Moreover, we have observed an increase in neurogenesis up to two months after the injury. These newborn neurons, however, present altered morphology and migration. CONCLUSIONS: In addition, we have found that NSCs get activated in higher numbers and acquire a reactive-like phenotype that is most likely caused by hyperexcitation. FINANCIAL SUPPORT: This project has received funding from the European Union’s Horizon 2020 research and innovation program under the Marie Skłodowska– Curie grant agreement no. 799384.