Objectives: 

Traumatic brain injury, especially in young people continues to be the most frequent cause of death and disability. In addition to being cause of death, its requiring long-term treatment and care increases the importance of developing new treatment options. In this study, optimization of the trauma injury model using different weights, in addition mechanism of post-traumatic injury and relationship with behavioral dysfunction have been evaluated.

Materials: 

An experimental rat model of traumatic brain injury is presented, in which standardized iron pellets (3, 7, 10 and 15 gram/ 6 mm in diameter) are dropped on the sensorimotor cortex from 50 cm. Impact of different weight of pellets resulted in different size of injury in cortex and underlying subcortical tissues as determined by Cresyl violet, DNA fragmentation. We have also analyzed behavioral abnormalities after traumatic brain injury.We have also analyzed phosphorylation of stress kinases, including p38 and JNK-1/2 which mediates cell death processes after brain injury.

Results: 

High frequency of mobility and increased anxiety that observed after injury was correlated with weight of pellets. Injury volume was 32±5, 28±3, 58±10 and 60±14 in animals subjected to impact with 3, 7, 10 and 15 gr pellets, respectively. In addition, increased degree of DNA fragmentation was observed especially in 10 and 15 gr pellets subjected animals.Increased phosphorylation of stress kinases were observed especially in animals subjected to 15 gram of pellet.

Conclusions: 

Our study indicates that different weight of pellets cause different size of injury, and behavioral abnormalities. The method establishes a clinically relevant, reproducible trauma model for the study of molecular mechanisms of traumatic brain injury in rats.