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Effects of repetitive low‐pressure explosive blast on primary neurons and mixed cultures
Author(s) -
Zander Nicole E.,
Piehler Thuvan,
Banton Rohan,
Benjamin Richard
Publication year - 2016
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23786
Subject(s) - glutamate receptor , calcium in biology , calcium , biophysics , intracellular , explosive material , in vitro , chemistry , traumatic brain injury , medicine , microbiology and biotechnology , biology , biochemistry , receptor , organic chemistry , psychiatry
Repetitive mild traumatic brain injury represents a considerable health concern, particularly for athletes and military personnel. For blast‐induced brain injury, threshold shock‐impulse levels required to induce such injuries and cumulative effects with single and/or multiple exposures are not well characterized. Currently, there is no established in vitro experimental model with blast pressure waves generated by live explosives. This study presents results of primary neurons and mixed cultures subjected to our unique in vitro indoor experimental platform that uses real military explosive charges to probe the effects of primary explosive blast at the cellular level. The effects of the blast on membrane permeability, generation of reactive oxygen species (ROS), uptake of sodium ions, intracellular calcium, and release of glutamate were probed 2 and 24 hr postblast. Significant changes in membrane permeability and sodium uptake among the sham, single‐blast‐injured, and triple‐blast‐injured samples were observed. A significant increase in ROS and glutamate release was observed for the triple‐blast‐injured samples compared with the sham. Changes in intracellular calcium were not significant. These results suggest that blast exposure disrupts the integrity of the plasma membrane, leading to the upset of ion homeostasis, formation of ROS, and glutamate release. Published 2016. †This article is a U.S. Government work and is in the public domain in the USA