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Behav Brain Res. 2018 Jul 16;347:148-157. doi: 10.1016/j.bbr.2018.03.007. Epub 2018 Mar 8.

Ultrastructural brain abnormalities and associated behavioral changes in mice after low-intensity blast exposure.

Author information

1
Department of Pathology & Anatomical Sciences, University of Missouri School of Medicine, Columbia, MO 65212, USA.
2
Department of Pathology & Anatomical Sciences, University of Missouri School of Medicine, Columbia, MO 65212, USA; Truman VA Hospital Research Service, Columbia, MO 65201, USA.
3
Department of Mining and Nuclear Engineering, Missouri University of Science and Technology, Rolla, MO 65409, USA.
4
Electron Microscopy Core Facility, University of Missouri, Columbia, MO 65211, USA.
5
Department of Biochemistry, University of Missouri School of Medicine, Columbia, MO 65212, USA.
6
Department of Radiology, Stanford University School of Medicine, Department of Electrical Engineering, Stanford University, Stanford, CA 94305, USA.
7
U.S. Naval Research Lab, Washington, DC 20375, USA.
8
Sidney Kimmel Institute for Nuclear Renaissance, Department of Physics and Astronomy, University of Missouri, Columbia, MO 65211, USA.
9
Canadian Military and Veterans' Clinical Rehabilitation, Faculty of Rehabilitation Medicine, University of Alberta, Edmonton, AB T6G 2G4, Canada.
10
Office of Research and Development, Department of Veterans Affairs, Washington, DC 20420, USA.
11
Department of Pathology & Anatomical Sciences, University of Missouri School of Medicine, Columbia, MO 65212, USA; Truman VA Hospital Research Service, Columbia, MO 65201, USA. Electronic address: guze@health.missouri.edu.

Abstract

Explosive blast-induced mild traumatic brain injury (mTBI), a "signature wound" of recent military conflicts, commonly affects service members. While past blast injury studies have provided insights into TBI with moderate- to high-intensity explosions, the impact of primary low-intensity blast (LIB)-mediated pathobiology on neurological deficits requires further investigation. Our prior considerations of blast physics predicted ultrastructural injuries at nanoscale levels. Here, we provide quantitative data using a primary LIB injury murine model exposed to open field detonation of 350 g of high-energy explosive C4. We quantified ultrastructural and behavioral changes up to 30 days post blast injury (DPI). The use of an open-field experimental blast generated a primary blast wave with a peak overpressure of 6.76 PSI (46.6 kPa) at a 3-m distance from the center of the explosion, a positive phase duration of approximate 3.0 milliseconds (ms), a maximal impulse of 8.7 PSI × ms and a sharp rising time of 9 × 10-3 ms, with no apparent impact/acceleration in exposed animals. Neuropathologically, myelinated axonal damage was observed in blast-exposed groups at 7 DPI. Using transmission electron microscopy, we observed and quantified myelin sheath defects and mitochondrial abnormalities at 7 and 30 DPI. Inverse correlations between blast intensities and neurobehavioral outcomes including motor activities, anxiety levels, nesting behavior, spatial learning and memory occurred. These observations uncover unique ultrastructural brain abnormalities and associated behavioral changes due to primary blast injury and provide key insights into its pathogenesis and potential treatment.

KEYWORDS:

Behavior; Blast wave; Blast-induced TBI; Neuropathology; Ultrastructural abnormalities

PMID:
29526786
DOI:
10.1016/j.bbr.2018.03.007
[Indexed for MEDLINE]

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