MID-TERM CELLULAR CONSEQUENCES OF SEVERE TRAUMATIC BRAIN INJURY IN MOUSE MODEL

Traumatic brain injury (TBI) is recognised as a chronic disease that constitutes a long-term risk factor for other neurological disorders. Histological and imaging observations in humans indicate that TBI induces a sustained neuroinflammatory response in the brain, as well as a delayed microglial response following the injury^1,2. Further evidence in mouse models supports the presence of persisting signs of neuroinflammation (astrogliosis and microgliosis) even long after severe or mild TBI^3,4. Here, in a model of severe TBI performed by controlled cortical impact in male mice, we investigated by immunohistochemistry the potential presence of a microglial and/or astroglial activation (Iba1 and GFAP immunostainings, respectively) 3 weeks post-injury. We also investigated whether TBI could induce mid-term activation of autophagy and endoplasmic reticulum stress (ERS), as these pathways are known to contribute to functional outcome after TBI. Our current data confirm the persistence of neuroinflammation three weeks after severe TBI, in particular regarding microglia activation in the site of injury. Our preliminary results also indicate that ERS is more important in the lesion site compared to the contralateral side and autophagy seems to be higher as well. Ongoing experiments are investigating further this characterization of key cellular events, as they may contribute to mid- and long-term pro-degenerative events associated to TBI.
1. Chodobski et al. (2011) Translational Stroke Research
2. Engel et al. (2000) Acta Neuropathologica
3. Vegliante et al (2019) Journal of Clinical Medicine
4. Drieu, et al (2022) Journal of Cerebral Blood Flow & Metabolism