A new in vivo animal model that produces
diffuse brain injuries in sagittal plane rearward rotational acceleration has been developed. In this model, the skull of an anesthetized adult rat is tightly secured to a rotating bar. During
trauma, the bar is impacted by a striker that causes the bar and the animal head to rotate rearward; the acceleration phase last 0.4 ms and is followed by a rotation at constant speed and a gentle deceleration when the bar makes contact with a padded stop. The total head angle change is less than 30°. By adjusting the air pressure in the rifle used to accelerate the striker, resulting rotational acceleration between 0.3 and 2.1 Mrad/s(2) can be produced. Numerous combinations of
trauma levels, post-
trauma survival times, brain and serum retrieval, and tissue preparation techniques were adopted to characterize this new model. The
trauma caused subdural bleedings in animals exposed to severe
trauma. Staining brain tissue with β-
Amyloid Precursor
Protein antibodies and FD Neurosilver that detect degenerating axons revealed wide spread axonal
injuries (AI) in the corpus callosum, the border between the corpus callosum and cortex and in tracts in the brain stem. The observed AIs were apparent only when the rotational acceleration level was moderate and above. On the contrary, only limited signs of
contusion injuries were observed following
trauma. Macrophage invasions,
glial fibrillary acidic protein redistribution or
hypertrophy, and blood brain barrier (BBB) changes were unusual. S100 serum analyses indicate that blood vessel and glia cell
injuries occur following moderate levels of
trauma despite the absence of obvious BBB
injuries. We conclude that this rotational
trauma model is capable of producing graded axonal injury, is repeatable and produces limited other types of
traumatic brain injuries and as such is useful in the study of injury biomechanics, diagnostics, and treatment strategies following
diffuse axonal injury.