TEMPOROSPATIAL PATTERNS OF GLIAL AND NEURONAL RESPONSES AFTER FOCAL UNILATERAL CORTICAL INJURY IN RATS

Traumatic brain injury (TBI) often leads to persistent motor impairments, yet the temporal and spatial tissue responses underlying these deficits remain incompletely understood. In this study, we examined glial and neuronal responses following focal cortical aspiration injury of the right hindlimb sensorimotor cortex in adult male rats, a model known to produce long-lasting gait asymmetry and postural deficits. Immunohistochemical analyses were conducted bilaterally in the peri-lesional cortex at 3, 7, 14, 21, and 28 days post-injury, targeting activated microglia/macrophages (CD11b, IBA1), astrocytes (GFAP), and neurons (NeuN). Following injury, we observed a rapid and spatially restricted accumulation of CD11b-positive myeloid cells in the injured hemisphere, consistent with early activation of resident microglia and infiltration of peripheral macrophages. This acute response was followed by a sustained IBA1-positive microglial reaction that progressively extended into the contralateral hemisphere over time. Astrocytic activation exhibited a delayed but prolonged profile, with ipsilateral GFAP upregulation emerging within the first week, peaking around two weeks post-injury, and becoming bilaterally elevated by four weeks. In contrast, sham-operated animals displayed only basal glial immunoreactivity without reactive morphology at any time point. NeuN immunoreactivity remained stable throughout the observation period, indicating preserved neuronal soma labeling and no evidence of overt secondary neuronal loss. Together, these findings demonstrate a staged and spatially differentiated glial response to focal cortical injury. This coordinated glial remodeling may contribute to persistent motor dysfunction after focal TBI and highlights glial–neuronal interactions as a potential target for therapeutic intervention.