Analysis of neuronal trauma and micro-tears in a rodent traumatic brain injury model

Exposure of military personnel to blast-pressure waves have increased within the last 10 years. These exposures induce traumatic brain injuries which can manifest in learning or memory deficits, post-traumatic stress disorder, or attention deficit disorder. To examine the histological changes that occur due to a blast exposure we assessed both Nissl- and GABAergic stained brain sections from a traumatic brain injury rodent model. Brain sections were examined for occurrences of micro-tears and areas of gross cellular damage following exposure to a 20 psi supersonic pressure wave directed from rostral to caudal. Neuronal degeneration was observed in discrete regions of the brain. A majority of degeneration was observed in the midbrain (medial parabrachial nuclei, ventrolateral tegmental region) and cortex (dentate gyrus, amygdala, and cortico-amygdalar transition zones. Lesser degrees of degeneration were observed in the Islands of Calleja and ventral pallidum. Regions with major micro-tear damage were primarily within cortex, the forebrain, and amygdala. Within cortex, damage was focused in auditory, somatosensory, piriform, and retrosplenial cortex. Smaller regions of more dispersed damage were also observed in motor and visual cortices. The location of micro-tears was more prominent in rostral sections of the brain and decreased in frequency as we moved caudally through the brain sections. Many micro-tears were dispersed throughout the affected brain regions; however clumps of tears were also noted. Both concentrated and dispersed regions of micro-tears were observed throughout all layers of cortex. Micro-tears ranged in size from small (3 µm) to large (25 µm). Sizes of micro-tears did not appear to depend on brain location, however a larger proportion of tears were observed near GABAergic neurons. The results correlate with behavioral phenotypes (e.g., tinnitus formation and depression) that are exhibited by blast-exposed animals in our model. Because the rodent behavioral data mimics the symptomology of blast-exposed humans, we hypothesize that micro-tears within cortical and amygdalar brain regions alter the function of various circuits in these regions. These alterations can potentially explain the myriad symptomology observed after blast-exposure in both rodent and human populations.