Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN, 47907, USA.
Department of Basic Medical Sciences, School of Veterinary Medicine, Purdue University, West Lafayette, IN, 47907, USA.
Sci Rep. 2022 Jul 12;12(1):11838. doi: 10.1038/s41598-022-14937-w.
While clinical observations have confirmed a link between the development of neurodegenerative diseases and traumatic brain injuries (TBI), there are currently no treatments available and the underlying mechanisms remain elusive. In response, we have developed an in vitro pendulum trauma model capable of imparting rapid acceleration injuries to neuronal networks grown on microelectrode arrays within a clinically relevant range of g forces, with real-time electrophysiological and morphological monitoring. By coupling a primary physical insult with the quantification of post-impact levels of known biochemical pathological markers, we demonstrate the capability of our system to delineate and investigate the primary and secondary injury mechanisms leading to post-impact neurodegeneration. Specifically, impact experiments reveal significant, force-dependent increases in the pro-inflammatory, oxidative stress marker acrolein at 24 h post-impact. The elevation of acrolein was augmented by escalating g force exposures (30-200 g), increasing the number of rapidly repeated impacts (4-6 s interval, 3, 5 and 10×), and by exposing impacted cells to 40 mM ethanol, a known comorbidity of TBI. The elevated levels of acrolein following multiple impacts could be reduced by increasing time-intervals between repeated hits. In addition, we show that conditioned media from maximally-impacted cultures can cause cellular acrolein elevation when introduced to non-impact, control networks, further solidifying acrolein's role as a diffusive-factor in post-TBI secondary injuries. Finally, morphological data reveals post-impact acrolein generation to be primarily confined to soma, with some emergence in cellular processes. In conclusion, this novel technology provides accurate, physical insults with a unique level of structural and temporal resolution, facilitating the investigation of post-TBI neurodegeneration.
虽然临床观察已经证实了神经退行性疾病的发展与创伤性脑损伤(TBI)之间存在关联,但目前尚无可用的治疗方法,其潜在机制仍难以捉摸。有鉴于此,我们开发了一种体外摆锤创伤模型,能够在临床相关的 g 力范围内对微电极阵列上生长的神经元网络施加快速加速损伤,并进行实时电生理和形态监测。通过将初始物理冲击与已知生化病理标志物的冲击后水平的定量相结合,我们展示了我们的系统能够描绘和研究导致冲击后神经退行性变的原发性和继发性损伤机制的能力。具体来说,冲击实验在冲击后 24 小时揭示了促炎、氧化应激标志物丙烯醛的显著、力依赖性增加。丙烯醛的升高通过增加 g 力暴露(30-200g)、增加快速重复冲击的次数(4-6s 间隔、3、5 和 10×)以及使受冲击的细胞暴露于 40mM 乙醇(TBI 的已知合并症)而增强。通过增加重复打击之间的时间间隔,可以降低多次打击后的丙烯醛水平升高。此外,我们表明,从最大冲击培养物中提取的条件培养基在引入非冲击对照网络时会引起细胞丙烯醛升高,这进一步证实了丙烯醛在 TBI 后继发性损伤中的扩散因子作用。最后,形态数据显示冲击后丙烯醛的产生主要局限于胞体,细胞突起中也有一些出现。总之,这项新技术提供了具有独特结构和时间分辨率的准确物理冲击,有助于研究 TBI 后的神经退行性变。