Traumatic Brain Injury (TBI) is known to impair motor coordination and affect cognitive functions. Parvalbumin-positive interneurons (PV-INs) are one subpopulation of GABAergic cells, which can balance their inhibitory output on connected pyramidal neurons, thereby influencing cortical network excitability. Here we investigated TBI-induced, morphological and functional changes of PV-Basket Cells (PV-BCs) in the ipsilateral hemisphere of somatosensory cortex and the underlying mechanisms. We used our established TBI model and performed immunohistochemistry, fluorescence in situ hybridization and electrophysiological recordings in acute brain slices of the ipsilateral somatosensory cortex. Sham-operated mice served as controls. Quantification of PV-positive cells using PV-fluorescence revealed a significant reduction in PV-IN density, with no morphological changes of surviving PV-BCs 24h after the injury. Electrophysiologically, we observed a reduced maximal firing frequency in PV-BCs after TBI. Since axonal HCN channels contribute to high-frequency firing in PV-BCs, we further investigated their functional expression. We observed increased HCN-channel mediated currents in PV-BCs post TBI. Furthermore, nucleated patch-clamp recordings disclosed a somatic expression of HCN channels in PV-BCs exclusively in the TBI group, while the levels of mRNA expression of HCN1/2 subunits were unaffected. Importantly, the maximal firing frequency of PV-BCs was similarly affected in presence of HCN-channel blocker in both groups. These data suggest that PV-BCs limit their maximal action potential firing frequency in the early phase after TBI by a spatial redistribution of HCN-channels from the axon to the somatic area, thereby likely contributing to cortical network hyperactivity.Supported by the German Research Foundation to T.M. (DFG, CRC1080, C02)