Traumatic brain injury (TBI) disrupts the complex arrangement of glia and neuronal cells in the central nervous system. Microglia, the resident immune cells, survey the cellular milieu under homeostatic conditions and play a neuroprotective role via clearance of dead cells and debris such as axons and myelin. Resting (ramified) microglia possess a distinct morphology—small rod-shaped somata with thin processes. After TBI, microglia are activated and transition into an amoeboid morphology. To delineate the spatiotemporal morphological response of microglia after TBI, we used a controlled cortical impact injury model to quantify and characterize microglia at 24 hr and 28 days after TBI in the hippocampus (H) and lateral posterior nucleus of the thalamus (LPNT). Increased numbers of microglia were observed in the H and LPNT at 28 days after controlled cortical impact, but not at 24 hr in comparison to controls. Spatially, controlled cortical impact resulted in an increase of amoeboid microglia bilaterally at 24 hr and 28 days in H and ipsilaterally in LPNT. Temporally, at 28 days, TBI resulted in a significant increase in the number of amoeboid microglia in both H and LPNT. In addition, at 28 days after injury, we observed an increase in translocator protein, a marker for activated microglia, in the ipsilateral thalamus only. TBI results in a spatiotemporal increase in amoeboid microglia in the hippocampus and the LPNT over 28 days. Delineating their spatiotemporal phenotype is critical because it can help identify therapeutic targets with appropriate therapy.
Keywords: TBI; cell death; inflammation; microglia; neuro degeneration; neuro glia; neuro immunity; neuro repair; therapies.