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Microglia polarisation in the rat thalamus and cerebellum after traumatic brain injury

Introduction: Neuropathophysiological cascade following traumatic brain injury (TBI) includes many complex processes and despite numerous preclinical and clinical studies, there is still no neuroprotective pharmacotherapeutic approach that could significantly improve clinical outcomes in patients. Neuroinflammation is considered to be one of the key processes in the TBI pathobiology. Therefore, better knowledge of microglial roles and activities could be very important for the development of new therapeutic strategies. The aim of this study was to determine the microglial/macrophages activation and possible signs of phenotypic “M1/M2” polarization in thalamus and cerebellum, within the first week after experimental TBI in the rat. Materials and methods: TBI of moderate severity was induced over the left parietal cortex using lateral fluid percussion injury (LFPI) and sham-operated animals were used as a control group. Rats were sacrificed 1, 3 or 7 days following TBI or sham procedure and their brains were prepared for immunohistological analyses. Double-staining of the brain slices was performed using primary antibody against ionized calcium binding adaptor molecule 1 (Iba1), in combination with anti-CD86, anti-CD206 or anti-Mac-2. Results: Microglia/macrophages with different morphology, observed in different time points in both thalamus and cerebellum, showed some colocalization with CD86 and CD206, but not with Mac-2 in the thalamus, while in cerebellum we did not detect any colocalization. Conclusions: Our preliminary results suggest that usage of “M1/M2” phenotypic polarization of microglia, originally described in in vitro studies, seems to have limited potential in experimental in vivo TBI research, at least with markers used in this study. This work has been supported by the University of Rijeka under the project uniri-biomed-18-204 to Ž.G.

Traumatic brain injury, microglia, thalamus, cerebellum, rat

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