Subacute Oxidative Stress and Glial Reactivity in the Amygdala are Associated with Increased Anxiety Following Blast Neurotrauma.
Subacute Oxidative Stress and Glial Reactivity in the Amygdala are Associated with Increased Anxiety Following Blast Neurotrauma.
复制标题
杏仁核中的亚急性氧化应激和神经胶质反应与爆炸性神经外伤后焦虑的增加有关。
DOI：
10.1097/shk.0000000000000311
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
VandeVord,PamelaJ
中科院分区：
文献类型：
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作者：
Sajja,VenkataSivaSaiSujith;Hubbard,WilliamB;VandeVord,PamelaJ
Behavioral symptoms, such as anxiety, are widely reported after blast overpressure (BOP) exposure. Amygdalar vulnerability to increasing magnitudes of BOP has not been investigated, and single exposures to blast have been limited to acute (< 72 h) assessment. Rats were exposed to a single low, moderate, or high BOP (10, 14, or 24 psi) with an advanced blast simulator to test the susceptibility of the amygdala. Anxiety-like behavior was observed in the low-and moderate-pressure groups when subjected to the light/dark box assessment 7 days after the blast but not in high-pressure group. Immunohistochemistry was performed to measure apoptosis (cleaved caspase-3), neuronal loss (NeuN), reactive astrocytes (glial fibrillary acidic protein), microglia (Iba-1), and oxidative stress (CuZn superoxide dismutase). Slower progression of injury cascades was associated with a significant increase in anxiety, apoptosis, and astrogliosis in the low pressure group compared with others. A significant increase of CuZn superoxide dismutase in the low pressure group could be associated with neuroprotection from cell death caused by oxidative stress because neuronal loss was significant in the moderate-and high-but not the low-pressure group. Overall, this study demonstrated that overpressure as low as 10 psi can induce subacute anxiety, in addition to neuropathologic changes in the amygdala.
