Traumatic brain injury (TBI) is termed a silent epidemic, with the US CDC reporting approximately 190 American deaths from TBI daily. The controlled cortical impact (CCI) model of TBI is the most accurate of the preclinical TBI models with controlled biomechanical injury parameters (displacement, speed, dwell time). CCI rats show motor and cognitive deficits as well as inflammation, oxidative stress, cell death, apoptosis, and gliosis in the brain.

Motor Deficits in CCI Rats

CCI animals show increased edema for 48 hours post injury (A). CCI animals show deficits in performance on the balance beam, exhibiting shorter balance times before they slip during the first week post-injury (B). Forelimb use is assessed using the cylinder test, which allows the quantification of the limb-use asymmetry. Animals with CCI lesion will present a significant impairment in the contralateral (right) forepaw use, demonstrating use asymmetry (C).

Cognitive Deficits in CCI Rats

Cognitive deficits in CCI rats appear 2-3 weeks post injury when tested in the Morris Water Maze (MWM) spacial memory task. CCI animals take longer to reach the platform (A) and swim longer distances (B) compared to sham animals. Interestingly no differences in the swim speed is seen between sham and CCI rats (C).

Lesion Size

A: Astroglia (GFAP) and microglia (Iba1) labeling counterstained for nuclei (DAPI, white) in a CCI and sham rat. The TBI (yellow dotted line) causes widespread pathology and neuroinflammatory response in the hippocampus (blue arrow). B: the lesion size in percent of the entire hemisphere is significantly larger in CCI rats. C: significant increase in hippocampal microglial cytosis in CCI rats

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