Abstract
Traumatic brain injury (TBI) has been designated as a signature injury of modern military conflicts. Blast trauma, in particular, has come to make up a significant portion of the TBIs which are sustained in warzones. Though most TBIs are mild, even mild TBI can induce long term effects, including cognitive and memory deficits. In our study, we utilized a mouse model of mild blast-related TBI (bTBI) to investigate TBI-induced changes within the cortex and hippocampus. We performed rapid Golgi staining on the layer IV and V pyramidal neurons of the parietal cortex and the CA1 basilar tree of the hippocampus and quantified dendritic branching and distribution. We found decreased dendritic branching within both the cortex and hippocampus in injured mice. Within parietal cortex, this decreased branching was most evident within the middle region, while outer and inner regions resembled that of control mice. This study provides important knowledge in the study of how the shockwave associated with a blast explosion impacts different brain regions.
Highlights
Traumatic brain injury (TBI) has been designated as a signature injury of modern military conflicts
Blast-related TBIs make up a significant portion of these injuries[8,9], accounting for numerous long term cognitive deficits in veterans who have been exposed to blasts
The same pattern was observed within the CA1 basilar tree of the hippocampus (Fig. 2b). This suggests that our model of mild blast-related TBI (bTBI) does result in a reduction in the distribution of the dendritic arbor
Summary
Traumatic brain injury (TBI) has been designated as a signature injury of modern military conflicts. In 2017, over 83,000 military personnel were diagnosed and treated for TBI by the U.S Department of Defense or the Veterans Administration[11] These injuries are often the result of exposure to an explosion which generates a blast shockwave that impacts the brain. Results consistently suggest decreases in neuronal density within the cortex and hippocampus on the ipsilateral side to the injury[20,21,22,23] This dendritic damage extends well beyond the area of injury; relatively minimal cell death still results in significant dendritic changes[24,25]. This may account for the cognitive deficits observed in both humans and animals exposed to a mild TBI. While there is significant evidence to suggest that even mild mechanical TBI induces relatively widespread dendritic changes, there have been few studies investigating these changes as a result of blast TBI
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