Neuroinflammatory Cascades Following Focal Cortical Injury Mirror the Progression of Motor Deficits in Rats

Traumatic brain injury (TBI) often leads to long-lasting motor deficits, yet the cellular mechanisms underlying these impairments remain incompletely understood. Here we examined glial and neuronal responses following focal ablation injury of the hindlimb sensorimotor cortex in adult male rats, a model previously shown to induce persistent gait asymmetry and postural deficits. Immunohistochemical analysis of resting and activated microglia, astrocytes, and neurons was performed bilaterally in peri-lesional cortex at 3, 7, 14, 21, and 28 days post-injury. The injury produced an early, sharply lo-calized increase in activated microglia and macrophages in the injured hemisphere, followed by sustained microglial activation that gradually extended contralaterally. Astrocytic activation displayed a delayed but more prolonged profile, rising ipsilater-ally within the first week, peaking around two weeks, and becoming bilaterally ele-vated by four weeks. Neuronal density and morphology were preserved throughout, indicating that motor impairments arose without secondary neuronal loss. These find-ings demonstrate a structured and temporally distinct cascade of glial responses mir-roring the evolution of motor deficits. The results suggest that focal cortical injury ini-tiates sequential inflammatory and astrocytic processes without secondary neuronal loss, highlighting glial–neuronal interactions as key targets for improving motor re-covery after TBI.