A behavioral and histological comparison of fluid percussion injury and controlled cortical impact injury to the rat sensorimotor cortex

Abstract

Our primary goal was to evaluate the behavioral and histological outcome of fluid percussion injury (FPI) and cortical contusion injury (CCI) to the sensorimotor cortex (SMC). The SMC has been used to evaluate neuroplasticity following CCI, but has not been extensively examined with FPI. In both the CCI and FPI models, a mechanical force of 4 mm in diameter was applied over the SMC, allowing for a direct comparison to measure the relative rates of histology and recovery of function in these models. Gross behavioral deficits were found on the sensory task (tactile adhesive removal task) and multiple motor assessments (forelimb asymmetry task, forelimb placing task, and rotorod). These sensorimotor deficits occurred in the absence of cognitive deficits in the water maze. The CCI model creates focal damage with a localized injury wheras the FPI model creates a more diffuse injury causing widespread damage. Both behavioral and histological deficits ensued following both models of injury to the SMC. The neuroplastic changes and ease at which damage to this area can be measured behaviorally make this an excellent location to assess traumatic brain injury (TBI) treatments. No injury model can completely mimic the full spectrum of human TBI and any potential treatments should be validated across both focal and diffuse injury models. Both of these injury models to the SMC produce severe and enduring behavioral deficits, which are ideal for evaluating treatment options.

Facilitating Mitochondrial Calcium Uptake Improves Activation-Induced Cerebral Blood Flow and Behavior after mTBI

“…This leads to tissue distortion and axonal shearing both proximal and distal to the injury location (Lindgren and Rinder, 1965 ; Dixon et al, 1987 ; McIntosh et al, 1989 ). In comparison to a more focal cortical contusion injury (CCI), lateral FPI induces significant cell death in distant regions even as far as the corresponding contralateral cortex (Peterson et al, 2015 ), and neurophysiological changes in deeper regions such as the hippocampus (Gupta et al, 2012 ; Li et al, 2015 ; Pang et al, 2015 ). In the current mTBI model, lateral FPI was performed in rats when they reached an age of 25–26 days according to the procedures established previously in our laboratory (Gupta et al, 2012 ; Li et al, 2015 ).…”

FGF20 protected against BBB disruption after traumatic brain injury by activating the AKT/GSK3β pathway to upregulate junction protein expression and inhibiting JNK/NFκB-dependent neuroinflammation

“…The CCI model is a stable and well-established animal model used to research TBI since 1988 [44]. Various parameters (velocity, depth, and dwell time) can be selected for CCI model development to achieve the required degree of injury with great reproducibility [45]. More importantly, this model exhibits relevant clinical TBI symptoms [46].…”

Converging early responses to brain injury pave the road to epileptogenesis

“…A majority of hilar neurons undergo subsequent degeneration over the course of a few days to a week due to secondary injury processes (Hunt et al, ; Toth et al, ). The focal impact of CCI generates more extensive loss of hippocampal pyramidal neurons than concussive injuries (Peterson, Maass, Anderson, Anderson, & Hoane, ). In contrast, the limited data on blast TBI suggests little acute cell loss within days after trauma (Kovacs et al, ).…”