engleski

Repetitive head trauma induces changes in the expression of some parameters of inflammation, stress and synaptic plasticity in the mouse frontal cortex and hippocampus

Repetitive mild traumatic brain injury (rmTBI) is a significant health problem especially important in certain populations such as the athletes and military personnel. Lately, it has been recognized that rmTBI possesses a potential to produce cumulative effects which lead to long-term consequences, including neurodegenerative disorders. The purpose of this research was to study the effects of rmTBI on some markers of inflammation, cellular stress and activity dependent synaptic plasticity in the frontal cortex and hippocampus of mice subjected to multiple mild head impacts using the weight drop model (Kane et al., 2012). Adult male mice were lightly anesthetized and subjected to head injuries two times daily, with 6-hour inter-injury intervals, for five days in a row. Sham-injured, control animals went through equivalent procedure as the rmTBI group, but without receiving the head impacts. Mice were sacrificed 1, 3 or 7 days after the last impact or sham injury and their frontal cortices and the hippocampi were prepared for Western blot analyses of the expressions of nuclear factor kappa B (NFκB), cyclooxygenase 2 (COX-2), heat shock protein 70 (HSP70) as well as postsynaptic density 95 (PSD95) and synaptophysin (SYP) proteins. rmTBI caused an increase in the cytosolic levels of NFκB in the frontal cortex and HSP70 in both frontal cortex and the hippocampus on the first day after the last trauma procedure, while there were no changes in the COX-2 expressions in the examined brain regions within the first week after the rmTBI. Regarding the expressions of synaptic plasticity related proteins, on the third day after the trauma procedures, increased cortical SYP expression and decreased hippocampal PSD95 levels were detected in the traumatized mice. Our preliminary study suggests that rmTBI in mice causes changes in some parameters of inflammation and cellular stress in the frontal cortex and hippocampus. These results also suggest that rmTBI induces some discreet synaptic changes in the examined brain regions in our experimental conditions. This research was supported by the Croatian Science Foundation grant IP-2016-06-4602 to G.Ž.

inflammation ; mouse ; repetitive traumatic brain injury ; synaptic plasticity

nije evidentirano