Citation

Woods AS, Colsch B, Jackson SN, Post J, Baldwin K, Roux A, Hoffer B, Cox BM, Hoffer M, Rubovitch V, Pick CG, Schultz JA, Balaban C. ACS Chem. Neurosci. 2013; 4(4): 594-600.

Affiliation

Structural Biology Unit, NIDA IRP, National Institutes of Health , Baltimore, Maryland, United States.

Copyright

(Copyright © 2013, American Chemical Society)

DOI

10.1021/cn300216h

PMID

23590251

Abstract

Explosive detonations generate atmospheric pressure changes that produce nonpenetrating blast induced "mild" traumatic brain injury (bTBI). The structural basis for mild bTBI has been extremely controversial. The present study applies matrix-assisted laser desorption/ionization (MALDI) mass spectrometry imaging to track the distribution of gangliosides in mouse brain tissue that were exposed to very low level of explosive detonations (2.5-5.5 psi peak overpressure). We observed major increases of the ganglioside GM2 in the hippocampus, thalamus, and hypothalamus after a single blast exposure. Moreover, these changes were accompanied by depletion of ceramides. No neurological or brain structural signs of injury could be inferred using standard light microscopic techniques. The first source of variability is generated by the Latency between blast and tissue sampling (peak intensity of the blast wave). These findings suggest that subtle molecular changes in intracellular membranes and plasmalemma compartments may be biomarkers for biological responses to mild bTBI. This is also the first report of a GM2 increase in the brains of mature mice from a nongenetic etiology.

Language: en