Inhibition of Neocortical Plasticity During Development by a Moderate Concussive Brain Injury

Abstract

To determine if a moderate traumatic brain injury (TBI) sustained early in life alters the capacity for developmental plasticity, 17-20-day-old rat pups received a lateral fluid percussion and then reared in an enriched environment for 17 days. Compared to sham-injured controls, this moderate TBI prevented the increase in cortical thickness (1.48 vs. 1.68 mm, p < 0.01) as well as the corresponding enhancement in cognitive performance in the Morris Water Maze (39 vs. 25 trials to criterion, p < 0.05). These injured animals exhibited no significant neuronal degeneration and no evidence of neurologic or motor deficits. These findings strongly support the conclusion that a diffuse brain injury is capable of inhibiting both anatomical and cognitive manifestations of experience-dependent developmental plasticity.

Effect of intracortical vascular endothelial growth factor infusion and blockade during the critical period in the rat visual cortex

“…The implantation-produced lesion induces a significantly lower increase of vascular density, which is one of the changes related to the postnatal maturation of the visual cortex (Argandoñ a and Lafuente, 1996Lafuente, , 2000Lafuente, , 2002Argandoñ a et al, 2005;Bengoetxea et al, 2008). Several authors have reported that brain injuries in developing animals generate a delay in plasticity without gross morphological damage (Prins et al, 1996;Fineman et al, 2000;Adelson et al, 2001;Argandoñ a et al, 2006;Gurkoff et al, 2006). We have found similar values when infusing vehicle or when blocking VEGF with an antibody.…”

Environmental Enrichment as a Viable Neurorehabilitation Strategy for Experimental Traumatic Brain Injury

“…Specifically, the effects of EE during development were assessed in rats subjected to a FP injury on postnatal days (PNDs) 17-20 and placed in EE for 17 days. 97 EE significantly increased cortical thickness in the frontal and occipital cortices of sham controls, relative to the STD shams, but did not increase cortical thickness after FP injury. EE also enhanced MWM performance in shams versus FP-injured rats in STD conditions, as would be expected, but did not improve behavior in the injured group.…”

“…106 In a paradigm where rats were placed in EE 1 week after a mid-line FP injury for 45 min per day (three times per week for 3 weeks for a total of nine sessions), no significant improvements in behavioral outcome were observed. 107 Moreover, EE did not restore MWM spatial learning, 97 or the latency to reach protective box and path length improvement on the Barnes maze. 83 A lack of EE-induced benefits was also noted for brain alterations, such as lesion volume 82 and neurotrophin levels.…”

“…These findings suggest that moderate concussive brain injuries in juveniles, albeit eliciting limited neuronal degeneration, attenuate outcomes of experience-dependent neural plasticity. 97 To further determine whether these anatomical and behavioral alterations during development in response to FP injury and EE, alone or in combination, correlate with changes in dendritic arborization, Ip and colleagues reported an ample description of dendritic analyses. 98 Briefly, PND 19 injured or sham rats were placed in either EE or STD housing on PND 20 for 17 days, followed by rehousing in STD environment until sacrifice on PNDs 47-51 for Golgi-Cox dendritic density and branching analysis in frontal, parietal, and occipital cortices.…”

Oxidative stress and modification of synaptic proteins in hippocampus after traumatic brain injury

“…Cortical contusion models of TBI result in cortical neuronal loss and altered function, growth, and plasticity of surviving neurons in non-cortical regions, many of which are involved in memory [21]. A persistent problem associated with TBI is impaired declarative memory, a hippocampal dependant cognitive task.…”