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Citation |
Hellewell SC, Ziebell JM, Lifshitz J, Morganti-Kossmann MC. Methods Mol. Biol. 2016; 1462: 253-266. |
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Affiliation |
Department of Epidemiology and Preventive Medicine, Monash University and Australian New Zealand Intensive Care Research Centre, Melbourne, VIC, Australia. |
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Copyright |
(Copyright © 2016, Holtzbrinck Springer Nature Publishing Group) |
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DOI |
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PMID |
27604723 |
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Abstract |
The 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. Language: en |