1 Center for Visual and Neurocognitive Rehabilitation, Atlanta VA Medical Center , Atlanta, Georgia .
2 Biomedical Engineering, Georgia Institute of Technology , Atlanta, Georgia .
J Neurotrauma. 2018 Sep 1;35(17):2104-2116. doi: 10.1089/neu.2017.5394. Epub 2018 Jul 2.
Acoustic blast overpressure (ABO) injury in military personnel and civilians is often accompanied by delayed visual deficits. However, most animal model studies dealing with blast-induced visual defects have focused on short-term (≤1 month) changes. Here, we evaluated long-term (≤8 months) retinal structure and function deficits in rats with ABO injury. Adult male Long-Evans rats were subjected to ABO from a single blast (approximately 190 dB SPL, ∼63 kPa, @80 psi), generated by a shock tube device. Retinal function (electroretinography; ERG), visual function (optomotor response), retinal thickness (spectral domain-optical coherence tomography; SD-OCT), and spatial cognition/exploratory motor behavior (Y-maze) were measured at 2, 4, 6, and 8 months post-blast. Immunohistochemical analysis of glial fibrillary acidic protein (GFAP) in retinal sections was performed at 8 months post-blast. Electroretinogram a- and b-waves, oscillatory potentials, and flicker responses showed greater amplitudes with delayed implicit times in both eyes of blast-exposed animals, relative to controls. Contrast sensitivity (CS) was reduced in both eyes of blast-exposed animals, whereas spatial frequency (SF) was decreased only in ipsilateral eyes, relative to controls. Total retinal thickness was greater in both eyes of blast-exposed animals, relative to controls, due to increased thickness of several retinal layers. Age, but not blast exposure, altered Y-maze outcomes. GFAP was greatly increased in blast-exposed retinas. ABO exposure resulted in visual and retinal changes that persisted up to 8 months post-blast, mimicking some of the visual deficits observed in human blast-exposed patients, thereby making this a useful model to study mechanisms of injury and potential treatments.
爆震冲击波过压（ABO）损伤在军事人员和平民中经常伴有延迟的视觉缺陷。然而，大多数处理爆炸引起的视觉缺陷的动物模型研究都集中在短期（≤1 个月）变化上。在这里，我们评估了 ABO 损伤大鼠的长期（≤8 个月）视网膜结构和功能缺陷。成年雄性长耳大鼠通过激波管装置接受来自单一爆震（约 190 dB SPL，≈63 kPa，@80 psi）的 ABO。在爆震后 2、4、6 和 8 个月测量视网膜功能（视网膜电图；ERG）、视觉功能（运动觉反应）、视网膜厚度（谱域光学相干断层扫描；SD-OCT）和空间认知/探索性运动行为（Y 迷宫）。在爆震后 8 个月对视网膜切片进行胶质纤维酸性蛋白（GFAP）的免疫组织化学分析。与对照组相比，爆震暴露动物的双眼的视网膜电图 a 波和 b 波、眼动电图、闪烁反应的振幅更大，潜伏期延迟。与对照组相比，爆震暴露动物的双眼对比敏感度（CS）降低，而空间频率（SF）仅在同侧眼降低。由于几个视网膜层的厚度增加，爆震暴露动物的双眼总视网膜厚度均大于对照组。年龄而不是爆震暴露改变了 Y 迷宫的结果。GFAP 在爆震暴露的视网膜中大大增加。ABO 暴露导致的视觉和视网膜变化持续到爆震后 8 个月，模拟了人类爆震暴露患者观察到的一些视觉缺陷，因此这是研究损伤机制和潜在治疗方法的有用模型。
