Citation

Baalman K, Cotton J, Rasband N, Rasband M. J. Neurotrauma 2013; 30(9): 741-751.

Affiliation

Baylor College of Medicine, Neuroscience, Houston, Texas, United States; kbaalman@bcm.edu.

Copyright

(Copyright © 2013, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2012.2478

PMID

23025758

Abstract

Exposure to a blast wave has been proposed to cause mild traumatic brain injury (mTBI), with symptoms including altered cognition, memory, and behavior. However, this idea remains controversial, and the mechanisms of blast-induced brain injury remain unknown. To begin to resolve these questions, we constructed a simple compressed air shock tube, placed rats inside the tube, and exposed them to a highly reproducible and controlled blast wave. Consistent with the generation of a mild injury, two weeks after exposure to the blast we found that motor performance was unaffected, and a panel of common injury markers showed little or no significant changes in expression in the cortex, corpus callosum, or hippocampus. Similarly, we were unable to detect elevated spectrin break-down products in brains collected from blast-exposed rats. However, using an object recognition task, we found that rats exposed to a blast wave spent significantly less time exploring a novel object when compared to control rats. Intriguingly, we also observed a significant shortening of the axon initial segment (AIS) in both the cortex and hippocampus of blast-exposed rats, suggesting altered neuronal excitability following exposure to a blast. A computational model showed that shortening the AIS increased both threshold and the interspike interval of repetitively firing neurons. These results support the conclusion that exposure to a single blast wave can lead to mTBI with accompanying cognitive impairment and subcellular changes in the molecular organization of neurons.

Language: en