• Sarah C Hellewell, Jenna M Ziebell, Jonathan Lifshitz, and M Cristina Morganti-Kossmann.
• Canadian Military and Veterans' Clinical Rehabilitation Research Program, Faculty of Rehabilitation Medicine, University of Alberta, 3-48, Corbett Hall, Edmonton, AB, Canada, T6G 2G4. hellewel@ualberta.ca.
• Methods Mol. Biol. 2016 Jan 1; 1462: 253-66.

AbstractThe impact acceleration (I/A) model of traumatic brain injury (TBI) was developed to reliably induce diffuse traumatic axonal injury in rats in the absence of skull fractures and parenchymal focal lesions. This model replicates a pathophysiology that is commonly observed in humans with diffuse axonal injury (DAI) caused by acceleration-deceleration forces. Such injuries are typical consequences of motor vehicle accidents and falls, which do not necessarily require a direct impact to the closed skull. There are several desirable characteristics of the I/A model, including the extensive axonal injury produced in the absence of a focal contusion, the suitability for secondary insult modeling, and the adaptability for mild/moderate injury through alteration of height and/or weight. Furthermore, the trauma device is inexpensive and readily manufactured in any laboratory, and the induction of injury is rapid (~45 min per animal from weighing to post-injury recovery) allowing multiple animal experiments per day. In this chapter, we describe in detail the methodology and materials required to produce the rat model of I/A in the laboratory. We also review current adaptations to the model to alter injury severity, discuss frequent complications and technical issues encountered using this model, and provide recommendations to ensure technically sound injury induction.

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