engleski

Lateral fluid percussion brain injury in the mouse: regional and temporal characterization of neuroinflammation

Traumatic brain injury (TBI) is the leading cause of morbidity and mortality worldwide so it represents a serious public health problem. The initial trauma is followed by complex pathophysiological responses that can cause further brain damage, among which inflammation is one of the key processes. In this study, our aim was to investigate inflammatory response in the parietal cortex as well as CA2, CA3 and dentate gyrus regions of the hippocampus at different time points after experimental TBI in the mouse. TBI of moderate severity was induced in adult male C57BL/6 mice by the lateral fluid percussion (LFP) brain injury model. In short, plastic Luer Lock fitting was attached to the craniotomy site over the left parietal cortex and this assembly was used to connect the animal to the LFP device and induce the brain injury. For the control group, sham-operated animals were used. Mice were sacrificed 3 or 14 days after the injury or sham procedure and their brains were prepared for immunohistological analyses. Primary antibodies against glial fibrillary acidic protein (GFAP), ionized calcium binding adaptor molecule 1 (Iba1) and Mac-2, which are astrocytic, microglial and activated microglia/macrophage markers, respectively, were used. In the parietal cortex, increased number of GFAP, Iba1 and Mac-2 positive cells at both studied time points after the TBI comparing to sham-injured animals was detected. The number of astrocytes and microglia was higher in all investigated hippocampal regions third day after LFP injury, but returned to the control levels at day 14, while no Mac-2 positive cells were present in hippocampus. Our preliminary results suggest marked inflammatory response in different brain regions third day after experimentally induced TBI in the mouse. In the parietal cortex, inflammation still persisted, but in the hippocampus it diminished two weeks after the injury.

traumatic brain injury; neuroinflammation; astrocytes; microglia; mouse

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