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

• Published in: Brain research 2006-03, Vol.1077 (1), p.24-36
• Main Authors: Gurkoff, Gene G., Giza, Christopher C., Hovda, David A.
• Format: Article
• Language: English
• Subjects: Age Factors; Animals; Biological and medical sciences; Brain Concussion - pathology; Brain Concussion - physiopathology; Cell Count; Cell death; Cell Death - physiology; Cerebral Cortex - growth & development; Cerebral Cortex - injuries; Cerebral Cortex - pathology; Cerebral Cortex - physiopathology; Disease Models, Animal; Dysfunction; Hippocampus; Hippocampus - growth & development; Hippocampus - injuries; Hippocampus - pathology; Hippocampus - physiopathology; Injuries of the nervous system and the skull. Diseases due to physical agents; Male; Maze Learning - physiology; Medical sciences; Morris water maze; Neurons - pathology; Random Allocation; Rats; Rats, Sprague-Dawley; Severity of Illness Index; Statistics, Nonparametric; Stereology; Traumas. Diseases due to physical agents; Traumatic brain injury
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2006.01.011

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