Lateral fluid percussion injury in the developing rat causes an acute, mild behavioral dysfunction in the absence of significant cell death

Lateral fluid percussion injury (LFP), a model of mild–moderate concussion, leads to the temporary loss of the capacity for experience-dependent plasticity in developing rats. To determine if this injury-induced loss in capacity for plasticity is due to cell death, we conducted stereological measurements within the cerebral cortex and CA3 of the hippocampus 2 weeks following mild, moderate or severe LFP in the post-natal day 19 (P19) rat. Results indicated that there was no significant change in the absolute number of neurons, regardless of injury severity, in either the ipsilateral cortex (sham = 10.6 ± 1.7, mild = 11.5 ± 2.1, moderate = 10.0 ± 1.0, severe = 10.9 ± 1.3 million neurons) or CA3 region of the hippocampus (sham = 251 ± 38, mild = 289 ± 2, moderate = 245 ± 48, severe = 255 ± 62 thousand neurons). Even though there was no evidence of a significant degree of injury-induced cell death, animals exhibited cognitive deficits as revealed in a Morris water maze task (MWM). The MWM results indicated that regardless of injury severity, P19-injured rats exhibited a significant increase in escape latency compared to age-matched shams (injury by day; P < 0.001) and a significant increase in the number of trials needed to reach criterion (P < 0.05). Analysis of a probe trial one week post-MWM training, however, indicated that there was no deficit in storage or recall of the learned behavior as analyzed by platform hits (sham = 2.9 ± 0.37, mild = 2.0 ± 0.40, moderate = 1 ± 0, severe = 2.8 ± 0.62) or percent time spent in, or immediately surrounding, the platform area (sham = 13.5 ± 1.71, mild = 10.8 ± 2.32, moderate = 12.7 ± 0, severe = 13.5 ± 1.69). Taken together, these results indicate that while LFP in P19-injured animals does not lead to significant cell death, it does generate acute, mild deficits in MWM performance.