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Blast‐induced neurotrauma leads to neurochemical changes and neuronal degeneration in the rat hippocampus
Author(s) -
Sajja Venkata Siva Sai Sujith,
Galloway Matthew P.,
Ghoddoussi Farhad,
Thiruthalinathan Dhananjeyan,
Kepsel Andrea,
Hay Kathryn,
Bir Cynthia A.,
VandeVord Pamela J.
Publication year - 2012
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/nbm.2805
Subject(s) - neurochemical , hippocampus , neuroscience , degeneration (medical) , neuronal degeneration , chemistry , medicine , biology , pathology , disease
Blast‐induced neurotrauma is a major concern because of the complex expression of neuropsychiatric disorders after exposure. Disruptions in neuronal function, proximal in time to blast exposure, may eventually contribute to the late emergence of clinical deficits. Using magic angle spinning 1 H MRS and a rodent model of blast‐induced neurotrauma, we found acute (24–48 h) decreases in succinate, glutathione, glutamate, phosphorylethanolamine and γ‐aminobutyric acid, no change in N ‐acetylaspartate and increased glycerophosphorylcholine, alterations consistent with mitochondrial distress, altered neurochemical transmission and increased membrane turnover. Increased levels of the apoptotic markers Bax and caspase‐3 suggested active cell death, consistent with increased FluoroJade B staining in the hippocampus. Elevated levels of glial fibrillary acidic protein suggested ongoing inflammation without diffuse axonal injury measured by no change in β‐amyloid precursor protein. In conclusion, blast‐induced neurotrauma induces a metabolic cascade associated with neuronal loss in the hippocampus in the acute period following exposure. Copyright © 2012 John Wiley & Sons, Ltd.