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Introduction: Millions of children and young adults are living with disabilities from traumatic brain injury (TBI) in childhood. Very little is known about age-dependent pathways of neuroplasticity on post-injury recovery. Hypothesis: We hypothesized that we could detect deficits in neuronal activity after TBI in the immature rat using electrophysiology recordings and functional magnetic resonance imaging (fMRI). Methods: Rats (P 16-18, n=10) underwent controlled cortical impact (CCI) to the left parietal cortex. Control rats (n=10) were age-matched, uninjured pups. Two weeks after CCI, the functional response of the uninjured (right) primary somatosensory cortex (S1) was measured with electrophysiology recording in response to left forepaw stimulation. Multi-unit activities (MUA) and local field potentials (LFP) were recorded with a 12-channel axial array electrode. The number of neuronal spiking events was calculated by post stimulus time histogram (PSTH) analysis of MUA. Rats also underwent blood oxygenation level dependent (BOLD) fMRI. Neuronal connections in the thalamo-cortical and cortical-cortical somatosensory pathways were evaluated by using manganese enhanced magnetic resonance imaging (MEMRI) and histology. Results: Electrophysiology recordings showed decreases in spiking rates across laminae II-V in the uninjured S1 of TBI rats (p<0.05). Stimulation on the left forepaw in TBI rats resulted in decreased LFP amplitude (laminae II-V) and increased LFP latency (laminae IV-V) in the uninjured S1 (p<0.05). Left forepaw stimulation also evoked decreases in the extent of fMRI responses in the uninjured S1 in TBI rats. MEMRI imaging did not show changes in the thalamo-cortical connections in the uninjured S1. However, luxo-blue staining showed decreases in the axon myelination volume along the corpus callosum connecting cortical-cortical somatosensory pathways (p<0.05, TBI vs controls). Conclusions: We conclude that TBI in immature rats adversely affects neuronal function of the contralateral (uninjured) S1 cortex, in part due to alterations in the cortical-cortical somatosensory pathways. These findings have implications for understanding recovery after pediatric TBI. Support: Johns Hopkins Brain Science Institute