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Citation
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Miyazaki H, Miyawaki H, Satoh Y, Saiki T, Kawauchi S, Sato S, Saitoh D. Acta Neurochir. (Wien) 2015; 157(12): 2111-20; discussion 2120. |
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Affiliation
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Division of Traumatology, Research Institute, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan. |
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Abstract
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BACKGROUND: Mild traumatic brain injury (mTBI) is caused by complex mechanisms of systemic, local and cerebral responses to blast exposure. However, the molecular mechanisms of cognitive impairment after exposure to blast waves are not clearly known. We tested the hypothesis that thoracic injury induced functional and morphological impairment in the brain, leading to behavioral abnormalities.
METHODS: Mice were exposed to laser-induced shock waves (LISWs) impacting the thorax and assessed for behavioral outcome at 7 and 28 days post injury. Hippocampus and lung were collected for histopathological analysis and gene expression profiling after injury.
RESULTS: Thoracic injury transiently decreased the heart rate, blood pressure, peripheral oxyhemoglobin saturation and cerebral blood flow immediately after LISW exposure. Although LISWs exposure caused pulmonary contusions, hemorrhage was not apparent in the brain. At 7 and 28 days after, the injured mice exhibited impaired short-term memory and depression-like behavior compared with controls. Histological assessments showed an increase in neuronal cell death after shock wave exposure, especially in the CA3 region of the hippocampus. Moreover, shock wave exposure altered the expression of functionally relevant genes in the hippocampus at 1 h and 1 day post injury.
CONCLUSIONS: Our findings indicate that the LISW-induced thoracic injury with no direct impact on the brain affected the hippocampal gene expression and led to morphological alterations, resulting in behavioral abnormalities. Therefore, body protection may be extremely important in the effective prevention against blast-induced alterations in brain function.
Language: en |