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Summary   Aims  Traumatic brain injury ( TBI ) occurs when the head is impacted by an external force causing either a closed or penetrating head injury through a direct or accelerating impact. In laboratory research, most of the  TBI  animal models focus on a specific region to cause brain injury, but traumatic injuries in patients do not always impact the same brain regions. The aim of this study was to examine the histopathological effects of different angles of mechanical injury by manipulating the trajectory of the controlled cortical impact injury ( CCI ) model in adult Sprague‐Dawley rats.    Methods  The  CCI  model was manipulated as follows: conventional targeting of the frontal cortex, farthest right angle targeting the frontal cortex, closest right angle targeting the frontal cortex, olfactory bulb injury, and cerebellar injury. Three days after  TBI , brains were harvested to analyze cortical and hippocampal cell loss, neuroinflammatory response, and neurogenesis via immunohistochemistry.    Results  Results revealed cell death in the M1 region of the cortex across all groups, and in the  CA 3 area from olfactory bulb injury group. This observed cell death involved upregulation of inflammation as evidenced by rampant  MHCII  overexpression in cortex, but largely spared Ki‐67/nestin neurogenesis in the hippocampus during this acute phase of  TBI .    Conclusion  These results indicate a trajectory‐dependent injury characterized by exacerbation of inflammation and different levels of impaired cell proliferation and neurogenesis. Such multiple brain areas showing varying levels of cell death after region‐specific  CCI  model may closely mimic the clinical manifestations of  TBI .

Brain Region‐Specific Histopathological Effects of Varying Trajectories of Controlled Cortical Impact Injury Model of Traumatic Brain Injury