We have recently demonstrated that fluid percussion injury (FPI) sustained early in life prevents the neural plasticity response associated with rearing in an enriched environment (EE). In order to determine if this reduction in plasticity capacity is reflected in alterations in dendritic arborization, the present study examined dendritic changes in response to EE, FPI, and FPI followed by EE. Twenty postnatal day 19-20 rat pups were subjected to FPI or sham injury and were subsequently housed in EE (17 days) or standard conditions. Brains were processed according to the Golgi-Cox method and were analyzed using dendritic density (Sholl) and dendritic branching analyses in frontal, parietal, and occipital cortices. Rearing in EE induced an increase in dendritic density, primarily within the occipital cortex. FPI induced an increase in dendritic density, primarily in regions remote from the injury site, namely contralateral parietal cortex and ipsilateral and contralateral occipital cortex. In injured animals subsequently housed in EE, FPI appeared to inhibit the experience-dependent dendritic density effects of EE. However, an unexpected enhancement of dendritic density was seen in the ipsilateral occipital cortex, indicating a unique response of this region based on its distance-specific sensitivity to injury-induced plasticity and its region-specific sensitivity to experience-dependent plasticity. These results suggest that dendritic changes mediate the anatomical and behavioral changes characteristic of impaired developmental plasticity following FPI, and that these changes are dependent on location within the cerebral cortex.