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 ¹H 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.
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