Citation

Tchantchou F, Puche AC, Leiste U, Fourney W, Blanpied TA, Fiskum G. J. Neurotrauma 2018; 35(10): 1192-1203.

Affiliation

University of Maryland School of Medicine , address , city, United States , postal code ; GFISKUM@anes.umm.edu.

Copyright

(Copyright © 2018, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2017.5401

PMID

29187028

Abstract

Many victims of blast traumatic brain injury (TBI) are occupants of vehicles targeted by land mines. A rat model of under-vehicle blast TBI was used to test the hypothesis that the neuropathology and altered behavior that ensue are mitigated by vehicle designs that dramatically reduce blast-induced acceleration (G force). Male rats were restrained on an aluminum platform that was accelerated vertically at up to 2850G, in response to detonation of an explosive positioned under a second platform in contact with the top via different energy-absorbing structures. The presence of polyurea-coated aluminum cylinders reduced acceleration by 80% to 550G compared to an 18% reduction by uncoated cylinders. Moreover, 67% of rats exposed to 2850G, and 20% of those exposed to 2350G died immediately after blast, whereas all rats subjected to 550G-blast survived. Assays for working memory (Y maze) and anxiety (Plus maze) were conducted for up to 28 days. Rats were euthanized at 24 h or 29 days post-blast and their brains used for histopathology and neurochemical measurements. Rats exposed to 2350G-blasts exhibited increased cleaved caspase-3 immunoreactive neurons in the hippocampus. There was also increased vascular IgG effusion and F4/80 immunopositive macrophages/microglia. Blast exposure reduced hippocampal levels of synaptic proteins bassoon and homer-1, which were associated with impaired performance in the Y maze and the Plus maze tests. These changes observed after 2350G-blasts were reduced or eliminated with the use of poly-urea coated cylinders. Such advances in vehicle designs should aid in the development of the next generation of blast-resistant vehicles.

Language: en

Keywords

Apoptosis; BLOOD-BRAIN BARRIER DYSFUNCTION; INFLAMMATION; SYNAPTIC LOSS AND DEAFFERENTATION; blood brain barrier